Cerebral ischemia model percutaneous puncture suture introduction method and device

Abstract

The invention relates to the technical field of experimental animal cerebral ischemia model construction, in particular to a cerebral ischemia model percutaneous puncture suture introduction method and a cerebral ischemia model percutaneous puncture suture introduction device, and the method comprises the following steps: percutaneous puncture of common carotid artery by a superfine puncture needle, withdrawal of the puncture needle after feeding into a micro catheter sheath through a needle cavity, and compression hemostasis by an external pressure type micro air bag ring. The suture is pushed to the starting section of the middle cerebral artery through the micro catheter sheath to complete embolism, the suture is withdrawn during reperfusion, air bag hemostasis is carried out again, and the device comprises a superfine puncture needle, the coaxial micro catheter sheath, a suture pushing core wire and an external pressure type micro air bag ring which form a three-layer nested structure, and the superfine puncture needle, the coaxial micro catheter sheath, the suture pushing core wire and the external pressure type micro air bag ring form a three-layer nested structure. The integrity of the blood vessels and the smoothness of the blood flow are completely retained after operation.

Description

Technical Field

[0001] This invention relates to the field of experimental animal cerebral ischemia model construction technology, specifically to a method and apparatus for percutaneous puncture suture insertion in cerebral ischemia models. Background Technology

[0002] Ischemic stroke is one of the leading causes of death and disability in humans, with approximately 15 million stroke events occurring globally each year. Ischemic stroke accounts for about 60% to 80% of all stroke cases. The middle cerebral artery occlusion (MCAO) suture embolism model is currently the most widely used animal model in basic research on cerebral ischemia. This model involves inserting a silicone-coated nylon suture into the intracranial cavity via the carotid artery to block the blood supply to the initial segment of the middle cerebral artery, thereby creating a controlled focal lesion of cerebral ischemia in the cerebral cortex and striatum.

[0003] The existing methods for preparing MCAO suture thrombus models mainly follow two classic technical routes: the Koizumi method and the Longa method. The Koizumi method, first reported in 1986, involves inserting a suture thrombus at the bifurcation of the common carotid artery (CCA) and pushing it through the internal carotid artery (ICA) to the origin of the middle cerebral artery. The Longa method is a modification of the Koizumi method, using the stump of the external carotid artery (ECA) as the insertion point. Both methods require a 3-4 cm longitudinal incision in the neck, layer-by-layer dissection of subcutaneous tissue and muscle, freeing the common carotid artery, internal carotid artery, and external carotid artery, and ligating and severing the external carotid artery and its branches (including the occipital artery, superior thyroid artery, lingual artery, and facial artery). Finally, the suture thrombus is inserted through the stump of the external carotid artery or the incision in the common carotid artery.

[0004] However, the aforementioned classic methods have the following technical drawbacks. First, the ligation and transection of the external carotid artery inevitably leads to the interruption of blood supply to the ipsilateral temporal and occipital regions. Studies have shown that approximately 47% of experimental rats developed ischemic myopathy in the external carotid artery supply area after online MCAO embolization, manifesting as temporalis muscle necrosis, masticatory dysfunction, and dysphagia, resulting in significant postoperative weight loss and deviations in motor function scores, severely interfering with the accuracy of cerebral ischemia injury assessment. Second, external carotid artery ligation leads to the complete loss of ipsilateral external carotid collateral circulation during the reperfusion phase. The brain tissue can only rely on the contralateral internal carotid artery and basilar artery through the Circle of Willis for compensatory blood supply. This compensatory reperfusion pattern is fundamentally different from the physiological reperfusion after endovascular thrombectomy in clinical patients, affecting the model's reference value for clinical translational research. Third, the operation of exposing and freeing the three major arteries in the neck requires delicate microsurgical techniques and a long surgical time. The separation of the vagus nerve and perivascular connective tissue is prone to causing collateral damage, increasing the incidence of postoperative complications and the mortality rate of experimental animals.

[0005] Chinese patent CN102908205A discloses a method for preparing a permanent middle cerebral artery occlusion (MCAO) model. This method uses spontaneously hypertensive rats and employs a suture occlusion method to establish a permanent MCAO model. The suture is inserted from the stump of the external carotid artery and pushed through the internal carotid artery to the origin of the middle cerebral artery. During the procedure, ligation of the external carotid artery and common carotid artery is required, which cannot avoid ischemia in the external carotid artery supply area. Chinese patent CN101023864A discloses a method for establishing a rat model of hemorrhagic cerebral infarction. It also uses the Longa method with suture insertion into the external carotid artery. The prepared suture is 0.235 mm in diameter and 30 to 40 mm in length, with one end heated to a smooth spherical shape. This method also requires incising to expose the neck vessels and ligating the external carotid artery. None of the above-mentioned patents involve a percutaneous puncture suture insertion route, nor do they propose solutions to avoid external carotid artery ligation.

[0006] Therefore, there is an urgent need to develop a minimally invasive MCAO modeling method and supporting device that can complete the insertion of sutures without cutting and exposing neck blood vessels or ligating the external carotid artery, so as to fundamentally overcome the ischemic complications in the external carotid artery supply area caused by the classic suture occlusion method and improve the clinical relevance of the cerebral ischemia model and the reliability of experimental data.

[0007] In recent years, although some researchers have attempted to improve reperfusion quality by replacing permanent ligation of the common carotid artery with carotid artery incision repair (CCA repair), this method repairs the vessel wall by covering the carotid artery incision with fibrin glue, but it still requires incising the neck to expose the vessel, and cannot fundamentally eliminate the risks of surgical trauma and damage to the external carotid artery branches. Another study reported a method of embolizing the middle cerebral artery using a microcatheter delivered via caudal artery puncture under fluoroscopic guidance. While this method achieves a percutaneous minimally invasive approach, it requires expensive X-ray fluoroscopy equipment, the zirconia ball embolization is an irreversible occlusion that cannot achieve reperfusion, and the residual embolic material in the intracranial vascular lumen may cause chronic foreign body reactions. None of the above-mentioned existing technologies simultaneously meet the three requirements of percutaneous minimally invasive operation, preservation of the integrity of external carotid artery blood flow, and reversible ischemia-reperfusion, leaving a clear technological gap. Summary of the Invention

[0008] To address the technical shortcomings of existing technologies that require cutting open and exposing the external carotid artery to ligate the MCAO suture thrombus model, resulting in the loss of ipsilateral temporal collateral circulation, this invention provides a percutaneous suture thrombus introduction method and device for a cerebral ischemia model.

[0009] The percutaneous puncture suture insertion method for a cerebral ischemia model includes the following steps: After anesthetizing the experimental animal, fix it in a supine position and disinfect the neck skin; under the guidance of a stereomicroscope, use an ultrafine puncture needle (27G to 33G, outer diameter not exceeding 0.41 mm) to directly puncture the common carotid artery percutaneously. The puncture site is located 1 to 3 mm proximal to the bifurcation of the common carotid artery. The puncture needle is inserted into the anterior wall of the common carotid artery at an insertion angle of 15° to 30°. Observe the blood return at the tail end of the puncture needle to confirm that the needle tip has entered the vascular lumen; insert a microcatheter sheath into the common carotid artery lumen through the puncture needle lumen, withdraw the puncture needle, and retain the microcatheter sheath; after the puncture needle is withdrawn, place an external pressure micro-inflatable ring on the skin surface corresponding to the puncture site and inflate it to 30 to 50%. mmHg, apply local compression to the puncture site on the anterior wall of the common carotid artery to stop bleeding; push the suture embolization through the microcatheter sheath along the common carotid-internal carotid artery path to the origin of the middle cerebral artery to complete the embolization; after the embolization is maintained for the predetermined ischemic time, withdraw the suture embolization through the same microcatheter sheath to achieve reperfusion; after the reperfusion is completed, remove the microcatheter sheath and apply external pressure micro-balloon ring for compression hemostasis again.

[0010] The percutaneous suture insertion device for a cerebral ischemia model includes an ultrafine puncture needle, a microcatheter sheath, and a suture pusher wire, which form a coaxial three-layer nested structure. The tip of the ultrafine puncture needle is ground into a bevel to reduce resistance when penetrating the blood vessel wall. The outer diameter of the microcatheter sheath is smaller than the inner diameter of the ultrafine puncture needle, and it can be inserted into the blood vessel lumen through the puncture needle cavity. The outer diameter of the suture pusher wire is smaller than the inner diameter of the microcatheter sheath, and its front end is connected to the suture head coated with silicone. The device also includes an external pressure micro-balloon ring, which includes a ring-shaped silicone balloon body and an inflation tube and a micro-injector connected to the ring-shaped silicone balloon body.

[0011] The beneficial effects of this invention are as follows: the percutaneous puncture path completely avoids neck incision and external carotid artery ligation, ensuring complete preservation of blood flow in the common carotid and external carotid arteries postoperatively, and preventing interference with collateral circulation in the temporal and occipital regions, thus eliminating approximately 47% of postoperative ischemic complications in the external carotid artery supply area associated with the classic suture occlusion method; hemostasis via the puncture needle tract utilizes external pressure micro-balloon rings for local compression, achieving natural hemostasis through elastic recoil of the vessel wall and platelet aggregation, eliminating the need for sutures or ligation, and achieving complete histological repair of the vessel wall at the puncture site within 28 days postoperatively, without intimal hyperplasia or... The lumen was narrowed; during the reperfusion phase, all three vascular pathways on the same side—the common carotid artery, external carotid artery, and internal carotid artery—remained patent, and the blood supply source for cerebral reperfusion was closer to the physiological reperfusion pattern after endovascular thrombectomy in patients with large vessel occlusion, thus improving the clinical translational value of the model; the operation time was shortened by about 50% compared to the traditional Longa method, the postoperative weight recovery rate of rats was significantly accelerated, and the experimental animals showed normal eating and drinking behavior after the operation, reducing the interference of confounding factors on the assessment results of cerebral ischemia injury and effectively improving the reliability and reproducibility of experimental data. Attached Figure Description

[0012] Figure 1 This is a schematic diagram of the overall structure of the percutaneous puncture suture insertion device of the present invention.

[0013] Figure 2 This is a radial cross-sectional schematic diagram of the coaxial three-layer nested structure of the present invention.

[0014] Figure 3 This is a schematic diagram of the external pressure micro airbag ring of the present invention.

[0015] Figure 4 This is a schematic diagram of the operation steps of the percutaneous suture insertion method of the present invention.

[0016] Among them, 1 is an ultra-fine puncture needle, 2 is the beveled tip of the needle, 3 is the needle hub, 4 is the coaxial microcatheter sheath, 5 is the tapered transition section, 6 is the micro Luer connector, 7 is the suture plug pusher wire, 8 is the flexible transition section, 9 is the suture plug head, 10 is the silicone coating, 11 is the nylon monofilament matrix, 12 is the external pressure micro-inflator ring, 13 is the annular silicone inflator body, 14 is the inflation tubing, 15 is the micro-injector, 16 is the common carotid artery, 17 is the internal carotid artery, 18 is the external carotid artery, 19 is the middle cerebral artery, and 20 is the puncture point. Detailed Implementation

[0017] The technical solution of the present invention will be described in detail below with reference to specific embodiments. These embodiments are only for illustrating the technical solution of the present invention and do not constitute a limitation on the scope of protection of the present invention.

[0018] In this invention, the ultrafine puncture needle refers to a puncture needle with a specification of 27G to 33G and an outer diameter not exceeding 0.41 mm, and its inner diameter of the needle lumen must meet the size requirements for the passage of the microcatheter sheath.

[0019] The percutaneous suture insertion method for cerebral ischemia model provided by this invention is based on the clinical percutaneous Seldinger puncture technique. It miniaturizes the mature three-step operation mode of percutaneous vascular puncture-catheter sheath placement-instrument delivery in clinical interventional therapy and transplants it into the preparation of experimental animal MCAO suture embolism model. Unlike the traditional Koizumi and Longa methods, which require cutting to expose the neck vessels and ligating the external carotid artery 18, this invention uses an ultra-fine puncture needle 1 to directly puncture the common carotid artery 16 percutaneously to establish a vascular access. The suture embolism is inserted through the coaxial microcatheter sheath 4, and the puncture needle tract is seamlessly closed and hemostatic by using an external pressure micro-balloon ring 12. The vascular integrity and blood flow of the common carotid artery 16, external carotid artery 18, and internal carotid artery 17 are not compromised throughout the entire operation.

[0020] Example 1: Percutaneous suture insertion method in a rat model of cerebral ischemia

[0021] This embodiment used adult male SD rats, weighing 260 to 300 g, provided by an SPF-grade animal breeding center. The rearing conditions were: temperature 22±1°C, relative humidity 50% to 60%, 12-hour light-dark cycle, and free access to water and food. All animal experimental procedures were reviewed and approved by the Laboratory Animal Ethics Committee, and the experimental operations complied with relevant national regulations on the management and use of laboratory animals.

[0022] Preparation of the percutaneous suture insertion device: such as Figure 1As shown, the puncture and insertion device used in this embodiment consists of four core components: an ultra-fine puncture needle 1, a coaxial microcatheter sheath 4, a suture pusher wire 7, and an external pressure micro-balloon ring 12. The ultra-fine puncture needle 1 is a 30G stainless steel injection needle with an outer diameter of 0.31 mm, an inner diameter of 0.17 mm, and an effective needle length of 20 mm. The needle tip is precision ground to a 12° to 18° bevel, preferably 15°. The bevel angle is chosen because: too small an angle (below 12°) results in an overly sharp needle tip that easily penetrates the posterior wall of the blood vessel, causing a penetrating injury; too large an angle (above 18°) increases resistance when penetrating the anterior wall, reducing the success rate of puncture. The needle body is made of 316L medical-grade stainless steel, and its surface roughness Ra value is reduced to below 0.2 μm through electrochemical polishing to reduce frictional resistance between the needle and the skin and blood vessel wall during puncture. The needle hub 3 is injection molded from polypropylene, and its outer wall has anti-slip textures for stable grip by the operator.

[0023] like Figure 2 As shown, the coaxial microcatheter sheath 4 is made of thin-walled polyimide tubing with an outer diameter of 0.24 to 0.28 mm (preferably 0.26 mm in this embodiment), an inner diameter of 0.18 to 0.22 mm (preferably 0.20 mm in this embodiment), a wall thickness of 0.02 to 0.04 mm (preferably 0.03 mm in this embodiment), and a length of 25 to 35 mm (preferably 30 mm in this embodiment). The distal end is machined into a 3° tapered transition section 5 with a length of 2 mm. The choice of polyimide material is based on its excellent mechanical properties and biocompatibility: the flexural modulus of this material is 3.0 to 3.5 GPa, which provides sufficient pushing stiffness to maintain the linear advancement of the microcatheter sheath 4 within the vascular lumen, while also possessing moderate flexibility to follow the natural curvature at the bifurcation of the common carotid artery 16; the water absorption rate of polyimide is less than 0.3%, exhibiting good dimensional stability in the blood environment and preventing the effective inner diameter of the lumen from decreasing due to water absorption and swelling. The proximal end of the microcatheter sheath 4 is equipped with a miniature Luer connector 6 with an outer diameter of 1.2 mm, which is used to fix and seal the proximal end of the microcatheter sheath 4 after the puncture needle 1 is withdrawn. The transition section allows the microcatheter sheath 4 to pass smoothly through the needle tip opening and the puncture hole in the vessel wall during the insertion of the puncture needle 1 into the blood vessel lumen, reducing damage to the vascular intima.

[0024] The suture pusher wire 7 is made of nickel-titanium alloy wire with a diameter of 0.12 mm and a total length of 40 mm. A flexible transition section 8, obtained through local heat treatment, is located 3 mm from the distal end. The superelastic properties of the nickel-titanium alloy allow the suture wire to passively follow the direction of the blood vessel's course and undergo elastic deformation without generating lateral thrust on the vessel wall when passing through the physiological curvature of the internal carotid artery 17. The flexible transition section 8 is prepared by subjecting the distal 3 mm of the suture wire to a 500°C salt bath for 15 minutes to lower its phase transformation temperature Af below body temperature, thus achieving a fully austenitic superelastic state under physiological conditions at 37°C. A silicone-coated suture plug is bonded to the front end of the suture wire using medical UV-curable adhesive. The suture plug substrate is 4-0 nylon monofilament 11 with a diameter of 0.16 mm. The tip 4 to 6 mm (preferably 5 mm in this embodiment) is coated with medical silicone, resulting in an outer diameter of 0.20 to 0.23 mm (preferably 0.21 mm in this embodiment). The silicone coating was prepared by dip-coating. During the coating process, the coating speed was controlled at 2 mm / s and the number of coatings was 3 to 4. After each coating, the coating was cured at room temperature for 30 min. The final coating thickness uniformity deviation did not exceed ±0.01 mm. The purpose of the coating was to increase the seal between the suture head 9 and the vessel wall of the initial segment of the middle cerebral artery 19 to ensure the embolization effect.

[0025] like Figure 3As shown, the structure of the external pressure micro-inflator ring 12 includes three parts: a ring-shaped silicone inflator body 13, an inflation tubing 14, and a micro-injector 15. The ring-shaped silicone inflator body 13 is made of medical-grade platinum-cured silicone, with a Shore A hardness of 30A, an inner diameter of 1.5 to 2.5 mm (preferably 2.0 mm in this embodiment), an outer diameter of 4 to 6 mm (preferably 5.0 mm in this embodiment), and a wall thickness of 0.4 mm. The inflator is a flat ring with a thickness of approximately 0.8 mm in the uninflated state. The platinum-cured silicone was chosen based on its excellent biocompatibility and mechanical reliability: the platinum-catalyzed cross-linking system contains no peroxide residue and will not irritate the skin contact surface; the silicone material has a tensile strength of 8 to 10 MPa and an elongation at break greater than 600%, capable of withstanding repeated inflation and deflation operations without fatigue rupture. The inner surface of the inflator body is coated with a hydrophilic polyvinylpyrrolidone coating of approximately 5 μm thickness after plasma treatment to increase the adhesion between the inflator and the skin surface and reduce slippage during operation. The inflation tubing 14 is a thin silicone tube with an inner diameter of 0.4 mm and a length of 150 mm. One end is connected to the side wall of the annular airbag 13, and the other end is connected to a micro-injector 15 with a volume of 0.3 mL. Injecting approximately 0.05 mL of air into the syringe inflates the airbag to a working pressure of 40 mmHg. This pressure value is based on the fact that the average systolic pressure of the rat common carotid artery 16 is approximately 120 to 140 mmHg. At the puncture site, the vessel wall has only a pinhole-sized defect, and the elastic recoil of the vessel wall itself can reduce the needle path to near closure. The 30 to 50 mmHg supplementary pressure provided by the external pressure airbag is sufficient to maintain effective hemostasis before the needle path is completely closed. Furthermore, this pressure level is far lower than the systolic pressure within the lumen of the common carotid artery 16, and will not cause compression of the common carotid artery 16 lumen, thus affecting the blood supply to the brain tissue.

[0026] Anesthesia protocol: Rats were weighed and induced with isoflurane inhalation anesthesia at an induction concentration of 4%, with an oxygen flow rate of 1.5 L / min. The maintenance concentration was 1.5% to 2.0%. Depth of anesthesia was assessed by monitoring the rats' withdrawal reflex to interdigital pinching stimuli. A heating pad was used throughout the procedure to maintain the rectal temperature at 37.0 ± 0.5°C. Isoflurane was chosen over chloral hydrate or sodium pentobarbital because isoflurane anesthesia offers better controllability, allowing for rapid adjustment of anesthesia depth through concentration control. Furthermore, the effects of isoflurane on cerebral ischemia-reperfusion injury have been well-characterized. Buprenorphine 0.05 mg / kg was administered subcutaneously 30 minutes preoperatively as prophylactic analgesia to reduce the interference of surgical stress on the experimental results.

[0027] Positioning and Neck Preparation: After anesthesia stabilized, the rats were fixed in a supine position on a specialized operating table, with their limbs secured with medical tape. The anterior neck area was prepared using an electric shaver, extending from the angle of the mandible to the supraclavicular fossa. After preparation, the area was disinfected three times with povidone-iodine solution, and a sterile surgical drape was laid to expose the anterior neck surgical area.

[0028] Stereomicroscopy localization: Adjust the stereomicroscope (magnification 8 to 40x) to face the anterior neck region of the rat. At 10 to 16x magnification, the pulsation location of the common carotid artery 16 can be clearly identified through the skin surface. The rat common carotid artery 16 is located approximately 2 to 3 mm lateral to the midline in the anterior neck region, running deep to the medial border of the sternocleidomastoid muscle. Palpation and visual confirmation of the location where the pulsation of the common carotid artery 16 is most prominent indicates the bifurcation region of the common carotid artery 16. The puncture site is selected approximately 2 mm proximal to the bifurcation of the common carotid artery 16. At this site, the diameter of the common carotid artery 16 is largest (approximately 1.0 to 1.2 mm), the vessel course is relatively straight, and there is sufficient safety distance from the bifurcation to avoid accidental insertion of the puncture needle into the external carotid artery 18 or internal carotid artery 17. Before determining the puncture site, a high-frequency Doppler ultrasound probe (frequency 20 MHz) was used to quickly scan the common carotid artery 16 to confirm the direction of the vessel, the inner diameter of the lumen, and the location of the bifurcation. Ultrasound-assisted localization can improve the accuracy of puncture site selection from 78% with simple visual palpation to more than 95%.

[0029] Percutaneous puncture procedure: such as Figure 4 As shown, the operator holds the 30G ultrafine puncture needle 1 with their dominant hand, with the bevel of the needle tip 2 facing upwards. The index and middle fingers of the non-dominant hand are used to gently press on both sides of the common carotid artery 16 for fixation. The puncture needle 1 is inserted at a 20° angle to the skin surface, approximately 1 mm from the tail end of the pulsation point of the common carotid artery 16, with the needle tip pointing towards the head, i.e., puncturing in the direction of blood flow. During insertion, the operator can feel the decreasing resistance as the needle tip penetrates the skin, a thin layer of subcutaneous muscle, and the adventitia-media-intima of the blood vessel. When the needle tip pierces the intima and enters the lumen, a small amount of bright red arterial blood can be seen oozing from the needle tail, forming a sign of backflow, confirming successful puncture. After successful puncture, the insertion angle is reduced to 10° to 15°, and the needle is further advanced approximately 1 mm along the long axis of the common carotid artery 16 to stabilize the needle tip within the blood vessel lumen. The entire puncture process should be completed within 10 seconds to minimize the retention time of the puncture needle 1 in the subcutaneous tissue and to reduce damage to surrounding tissues.

[0030] Insertion of microcatheter sheath 4: After confirming successful puncture, fix the puncture needle 1 with the non-dominant hand, and use microforceps with the dominant hand to grasp the proximal end of the microcatheter sheath 4. Slowly insert the tapered distal end of the microcatheter sheath 4 along the lumen of the puncture needle 1. After the distal end of the microcatheter sheath 4 enters the lumen of the common carotid artery 16 from the needle tip opening, continue to advance it for about 5 mm to ensure that the distal end of the microcatheter sheath 4 has sufficient anchoring length in the vessel lumen. During insertion, maintain a uniform and slow advancement speed, controlled at 1 to 2 mm / s, to avoid rapid advancement that could cause shear damage between the distal end of the microcatheter sheath 4 and the vessel intima. Then, slowly withdraw the puncture needle 1 while keeping the microcatheter sheath 4 in the same position, completing the exchange of puncture needle 1 and microcatheter sheath 4. A small amount of bleeding will occur around the puncture tract the moment the puncture needle 1 is withdrawn. At this time, the pre-prepared external pressure micro-balloon ring 12 is immediately placed on the skin surface corresponding to the puncture point 20. Air is injected using a micro-syringe 15 to inflate the ring balloon 13 to 40 mmHg. The balloon applies uniform radial pressure to the puncture point 20 on the anterior wall of the common carotid artery 16 from the skin surface. Under the pressure of the balloon, the smooth muscle of the blood vessel wall around the puncture tract elastically retracts, causing the puncture tract to gradually narrow. At the same time, platelets in the blood flow adhere, activate, and aggregate on the exposed subendothelial collagen fibers at the edge of the puncture tract, forming a stable platelet embolus to seal the puncture tract defect within 3 to 5 minutes. The compression duration is 3 to 5 minutes, and the balloon compression area covers the puncture tract and its surrounding area within 0.5 to 1.0 mm, achieving natural hemostasis.

[0031] Embolization and suture insertion: After confirming hemostasis at puncture point 20 (and observing no active bleeding after releasing the balloon after 5 minutes of compression), the suture insert 7 is inserted into the common carotid artery 16 through the microcatheter sheath 4. During insertion, the operator uses tactile feedback to judge the direction of suture advancement and changes in resistance. The suture head 9 advances cephalad along the lumen of the common carotid artery 16. When it reaches the bifurcation of the common carotid artery 16, it should be gently manipulated to selectively insert the suture head 9 into the internal carotid artery 17 rather than the external carotid artery 18. The key point here is that the internal carotid artery 17 is a direct continuation of the common carotid artery 16 and has a larger diameter. Without lateral deflection, the suture tends to enter the internal carotid artery 17 along the main blood flow direction. If the suture head 9 mistakenly enters the external carotid artery 18 (manifested as increased advancement resistance at the superficial layer), it should be gently withdrawn 2 to 3 mm and the suture rotation angle adjusted before being pushed again. The suture continues through the internal carotid artery 17, passing through the opening of a branch of the pterygopalatine artery (care must be taken to avoid accidentally entering the pterygopalatine artery here), and reaches the origin of the anterior cerebral artery through the intracranial segment of the internal carotid artery 17, thereby blocking the blood supply to the origin of the middle cerebral artery 19. The total insertion depth of the suture from the puncture point 20 to the origin of the middle cerebral artery 19 is approximately 17 to 20 mm (typically 18 to 19 mm in this embodiment) (measured from the bifurcation of the common carotid artery 16). When the operator feels slight elastic resistance, it indicates that the head of the suture 9 has reached the origin of the middle cerebral artery 19, at which point pushing should be stopped. Immediate verification of successful embolization can be achieved by monitoring the surface blood flow of the ipsilateral cerebral cortex using a laser Doppler flowmeter. When embolization is successful, the cortical blood flow should decrease to less than 20% of the baseline level.

[0032] Ischemia Maintenance and Reperfusion: After the suture plug is in place, the positions of the microcatheter sheath 4 and the suture plug pusher wire 7 remain unchanged. The proximal end of the microcatheter sheath 4 is fixed to the skin surface of the rat's neck with medical tape. The ischemia maintenance time is set according to the experimental design requirements; the transient ischemic-reperfusion model is usually maintained for 60 to 90 minutes. During ischemia maintenance, the depth of anesthesia and rectal temperature are continuously monitored, and heart rate and respiratory rate are recorded every 15 minutes to ensure that vital signs are within the normal physiological range. After the ischemia time is reached, the suture plug pusher wire 7 is slowly withdrawn so that the suture plug head 9 is withdrawn back into the lumen of the common carotid artery 16 (the withdrawal distance is approximately the full length of the insertion depth). The withdrawal speed is controlled at 1 mm / s to avoid rapid withdrawal that may cause damage to the vascular intima or induce vasospasm. Subsequently, the suture plug pusher wire 7 is completely withdrawn from the microcatheter sheath 4. After the suture plug is withdrawn, bright red blood can be observed flowing out through the lumen of the microcatheter sheath 4, indicating that blood flow from the internal carotid artery 17 to the middle cerebral artery 19 has been restored. Laser Doppler flowmeter monitoring showed that ipsilateral cortical blood flow recovered to 60% to 80% of the baseline level within 5 to 10 minutes after the thrombus was removed. This recovery rate is higher than the 45% to 65% of the traditional Longa method. This is because the method preserves the collateral communication between the external carotid artery 18 and the internal carotid artery 17.

[0033] Withdrawal of microcatheter sheath 4 and final hemostasis: After confirming reperfusion, slowly withdraw the microcatheter sheath 4. Immediately after withdrawal, reposition the external pressure micro-balloon ring 12 at the corresponding position of puncture point 20 and inflate to 40 mmHg for a second compression hemostasis. Since the puncture tract has already undergone platelet aggregation and preliminary fibrin deposition during the first hemostasis, the second puncture (microcatheter sheath 4 enters and exits through the original puncture tract) causes less damage to the puncture tract wall, and the time required for the second hemostasis is usually 2 to 3 minutes. After hemostasis is completed, release the balloon pressure, observe for 3 minutes to confirm no active bleeding, and then remove the balloon ring 12. Disinfect the skin in the anterior neck area with povidone-iodine; no sutures are required (puncture point 20 is only a needle-sized skin defect that can heal spontaneously). Stop isoflurane inhalation, and after the rat regains spontaneous activity, return it to its cage. Administer buprenorphine 0.05 mg / kg subcutaneously every 12 hours for three consecutive days post-surgery for analgesia management.

[0034] Example 2: Device Parameter Optimization

[0035] Based on Example 1, this example conducts a systematic optimization experiment on the key parameters of the percutaneous puncture suture insertion device.

[0036] Optimization of puncture needle 1 specifications: Four specifications of puncture needle 1, namely 27G (outer diameter 0.41 mm), 29G (outer diameter 0.34 mm), 30G (outer diameter 0.31 mm) and 32G (outer diameter 0.24 mm), were tested, with 25 rats in each group. The results showed that the 27G puncture needle 1 had excessively large puncture site, resulting in significant bleeding after withdrawal, with an average bleeding volume of 0.12±0.04 mL. The time required for hemostasis by balloon compression was prolonged to 10.3±1.8 min, and two rats developed hematomas at the puncture site 20, requiring manual compression for hemostasis. The 29G puncture needle 1 had a bleeding volume of 0.06±0.02 mL, a hemostasis time of 7.1±1.5 min, and a puncture success rate of 88% (22 / 25). The 30G puncture needle 1 had a bleeding volume of only 0.02±0.01 mL, a hemostasis time of 4.2±0.8 min, and a puncture success rate of 92% (23 / 25). The 32G puncture needle 1 had an inner diameter that was too small (0.11 mm), preventing the passage of the 0.26 mm outer diameter microcatheter sheath 4. Considering the puncture success rate, hemostasis time, and compatibility with the microcatheter sheath 4, the 30G puncture needle 1 achieved the best balance.

[0037] Material optimization of microcatheter sheath 4: Microcatheter sheaths 4 made of three materials—polyimide (PI), polyetheretherketone (PEEK), and polytetrafluoroethylene (PTFE)—were tested, with 20 rats in each group. The PI sheath, with the thinnest wall thickness (0.03 mm), achieved the largest inner diameter and a bending stiffness of 0.18 N·mm. 2The pipe exhibits good deformation compliance when passing through the 16th bifurcation bend of the common carotid artery; the bending stiffness of the PEEK pipe is 0.35 N·mm. 2 The high stiffness of the PTFE tubing poses a risk of excessive support force and localized pressure on the vessel wall when passing through curved sections. In the experiment, one rat experienced minor intimal abrasion at the entrance of the internal carotid artery at point 17. PTFE tubing has the lowest coefficient of friction (0.04), but its large wall thickness (0.05 mm) reduces the usable inner diameter to 0.16 mm, limiting the size options for the suture pusher wire 7. Based on comprehensive evaluation, PI material was selected as the preferred material for the microcatheter sheath 4.

[0038] Optimization of airbag compression pressure: The inflation pressure of the external pressure micro-airbag ring 12 was set to five levels: 20, 30, 40, 50, and 60 mmHg, with 10 rats in each group. At a pressure of 20 mmHg, 3 rats experienced persistent bleeding at the puncture site 20, requiring secondary hemostasis. Within the range of 30 to 50 mmHg, all rats achieved effective hemostasis within 5 minutes, with the 40 mmHg group having the shortest hemostasis time, averaging 3.8 ± 0.6 minutes. At 60 mmHg, although hemostasis was rapid (average 2.5 ± 0.4 minutes), 2 rats experienced a transient decrease in blood flow in the ipsilateral common carotid artery 16 (laser Doppler monitoring showed a transient decrease in cortical blood flow to 85% of baseline), suggesting that excessive external pressure may cause transient compression and stenosis of the common carotid artery 16 lumen. Therefore, 40 mmHg was determined as the recommended working pressure, and adjustments can be made within the range of 30 to 50 mmHg based on actual bleeding conditions if necessary.

[0039] Optimization of suture coating parameters: The coating length and outer diameter after coating of silicone-coated sutures were optimized. Sutures with coating lengths of 3, 4, 5, and 6 mm, and outer diameters of 0.19, 0.21, and 0.23 mm after coating, were prepared respectively. Embolization success rate (cortical blood flow decreased to below 20% of baseline) and incidence of subarachnoid hemorrhage were used as evaluation indicators. The results showed that the combination of a 5 mm coated segment and a 0.21 mm outer diameter after coating had the highest embolization success rate (96%, 24 / 25) and the lowest incidence of subarachnoid hemorrhage (4%, 1 / 25). The embolization success rate of the suture with a 0.23 mm outer diameter after coating was also 96%, but the incidence of subarachnoid hemorrhage increased to 12% (3 / 25). This was because the thicker suture head 9 generated a greater lateral thrust when it bent through the intracranial segment of the internal carotid artery 17. The embolization success rate of the suture with a 0.19 mm outer diameter after coating was only 76% (19 / 25), suggesting that the diameter of the suture head 9 was insufficient to completely block the blood flow in the initial segment of the middle cerebral artery 19.

[0040] Example 3: Model Performance Verification

[0041] This embodiment presents a parallel comparative experiment between the percutaneous suture occlusion method (the method of this invention) and the traditional Longa suture occlusion method. The experimental animals were adult male SD rats, weighing 270 to 290 g, which were randomly divided into a percutaneous puncture group (n=15) and a traditional Longa group (n=15), with the ischemia time set at 90 min for both groups.

[0042] Comparison of operation time: The average operation time from the start of skin disinfection to the placement of the suture and completion of embolization was 12.3±2.1 min in the percutaneous puncture group, and 25.6±4.3 min in the conventional Longa group. The operation time in the percutaneous puncture group was significantly shorter (P<0.01). The shortened time was mainly due to the omission of steps such as neck incision, vascular dissection, ligation and transection of the external carotid artery 18.

[0043] Neurological function assessment: Neurological deficits were assessed using the Longa 5-point scale 24 hours post-operation. The mean score in the percutaneous puncture group was 2.67±0.49, and in the traditional Longa group it was 2.73±0.59. There was no statistically significant difference between the two groups (P>0.05), indicating that the cerebral ischemia models established by the two methods were comparable in terms of the degree of neurological deficit. At 72 hours post-operation, a more refined neurological function assessment was performed using the modified neurological severity score (mNSS). The mNSS score in the percutaneous puncture group was 9.2±1.3 (out of 18), and in the traditional Longa group it was 9.5±1.6. Again, there was no statistically significant difference between the two groups (P>0.05).

[0044] Infarct volume: Rats were sacrificed 24 hours post-surgery, and their brains were harvested. 2 mm thick coronal sections were prepared and stained with 1% TTC solution at 37°C for 15 min. Normal brain tissue appeared bright red, while the infarcted area appeared pale white. ImageJ software analysis calculated the percentage of infarct volume to the ipsilateral hemisphere. The percentage was 38.2% ± 5.7% in the percutaneous puncture group and 36.5% ± 6.4% in the conventional Longa group, with no statistically significant difference between the two groups (P>0.05). The infarcted areas mainly involved the frontoparietal lobe and striatum of the ipsilateral cerebral cortex, and the distribution and morphological characteristics of the infarct foci were highly consistent between the two groups. The coefficient of variation (CV) of infarct volume in the percutaneous puncture group was 14.9%, lower than the 17.5% in the conventional Longa group, suggesting a slight advantage in the consistency of infarct volume in the percutaneous puncture model.

[0045] Assessment of the external carotid artery 18 supply area: Twenty-four hours post-surgery, before euthanasia, a cervical MRI was performed to assess the tissue status of the external carotid artery 18 supply area. In the conventional Longa group, 7 rats (7 / 15, 46.7%) showed high signal intensity in the ipsilateral temporalis and / or masseter muscle region on T2-weighted images, indicating ischemic injury; in the percutaneous puncture group, none (0 / 15, 0%) showed the above abnormal signal, and the difference between the two groups was statistically significant (P<0.001). Histological HE staining further confirmed that the temporalis muscle specimens of rats with abnormal MRI signals in the conventional Longa group showed typical pathological changes of acute ischemic myopathy, such as myofibril edema, eosinophilic degeneration, and interstitial inflammatory cell infiltration, while the temporalis muscle tissue structure in the percutaneous puncture group was completely normal. Immunohistochemical staining was used to detect the expression of the ischemic marker CD68 (macrophage marker). The density of CD68 positive cells in the temporalis muscle of rats in the traditional Longa group was 42.3±8.7 cells / high power field, while the density of CD68 positive cells in the temporalis muscle of the percutaneous puncture group was only 3.1±1.2 cells / high power field. The difference was statistically significant (P<0.001).

[0046] Postoperative weight recovery: Rats' weight changes were monitored for 7 consecutive days post-surgery. The conventional Longa group showed significant weight loss from day 1 to 3 post-surgery, with a maximum average weight loss of 8.3% ± 2.1% of baseline weight, and had not recovered to preoperative weight levels by day 7. The percutaneous puncture group showed a significantly smaller postoperative weight loss, with a maximum average loss of 3.5% ± 1.2% (P < 0.01), and recovered to preoperative weight levels by day 5. This difference in weight recovery is attributed to the preservation of the intact external carotid artery 18 blood supply in the percutaneous puncture group, which did not affect the rats' chewing and swallowing functions, and resulted in normal feeding and drinking behavior post-surgery. Further monitoring of feed consumption showed that the average daily feed consumption per rat in the percutaneous puncture group was 18.5 ± 3.2 g from day 1 to 3 post-surgery, while it was only 11.3 ± 4.1 g in the conventional Longa group (P < 0.01), further supporting the protective effect of the integrity of the external carotid artery 18 blood supply area on postoperative feeding function.

[0047] Reperfusion blood flow recovery: The recovery of cortical blood flow in the two groups of rats after suture removal was compared using a laser speckle flow imaging system. Ten minutes after suture removal, the ipsilateral cortical blood flow recovery rate in the percutaneous puncture group was 73.5% ± 8.2% of baseline, compared to 52.1% ± 10.6% in the conventional Longa method (P < 0.01). Sixty minutes after reperfusion, the blood flow recovery rate in the percutaneous puncture group was 82.8% ± 6.3%, compared to 61.4% ± 9.8% in the conventional Longa method (P < 0.01). The significantly higher reperfusion blood flow recovery rate in the percutaneous puncture group was attributed to the complete preservation of the collateral circulation pathway between the ipsilateral external carotid artery 18 and internal carotid artery 17, especially the retrograde blood supply from the external carotid artery 18 to the intracranial segment of the internal carotid artery 17 via the ophthalmic artery anastomosis, which was completely lost in the conventional Longa method due to ligation of the external carotid artery 18. Further monitoring data 24 h after reperfusion showed that the percutaneous puncture group maintained stable cortical blood flow at 78.6% ± 5.8% of baseline, while the conventional Longa group showed a secondary decrease in blood flow (down to 54.3% ± 11.2% of baseline) 6 to 12 h after reperfusion. This phenomenon may be related to the delayed hypoperfusion caused by the lack of collateral circulation in the conventional method.

[0048] Example 4: Applicability Validation of Mouse Model

[0049] To verify the applicability of the method of this invention to different species of experimental animals, this embodiment used adult male C57BL / 6 mice weighing 23 to 28 g as experimental subjects. The diameter of the common carotid artery 16 in mice is approximately 0.5 to 0.6 mm, significantly smaller than that in rats (1.0 to 1.2 mm), which places higher demands on the miniaturization of the puncture device. Considering the anatomical characteristics of mice, the puncture needle 1 was replaced with a 33G specification (outer diameter 0.21 mm, inner diameter 0.11 mm), the outer diameter of the microcatheter sheath 4 was reduced to 0.18 mm (wall thickness 0.02 mm), the outer diameter of the suture plug pusher wire 7 was 0.08 mm, and the outer diameter of the suture plug head 9 after coating was 0.17 mm. Due to the smaller diameter of the common carotid artery 16 in mice, puncture was more difficult, and the success rate was 80% (16 / 20), lower than the 92% in the rat model. Sixteen mice that underwent successful percutaneous puncture were subjected to 60 min of ischemia-reperfusion. At 24 h post-procedure, TTC staining showed that the infarct volume as a percentage of the ipsilateral hemisphere was 35.8% ± 7.2%, which was not statistically different from the infarct volume of the conventional Longa method mouse model under the same conditions (33.6% ± 8.5%) (P>0.05). The postoperative ischemia rate in the external carotid artery 18 supply area of ​​the mouse model was also 0% (0 / 16), further confirming the advantage of percutaneous puncture in preserving the integrity of blood flow in the external carotid artery 18 in different animal species.

[0050] Example 5: Long-term follow-up and model stability evaluation

[0051] This embodiment describes a long-term follow-up observation of a rat cerebral ischemia-reperfusion model established by percutaneous suture occlusion for 28 days post-surgery. The experimental animals were adult male SD rats, weighing 270-290 g, with 20 rats in each of the percutaneous puncture group and the conventional Longa group. The ischemia time was 90 min. Neurological function assessment, weight monitoring, and behavioral tests were performed on postoperative days 1, 3, 7, 14, 21, and 28.

[0052] Long-term neurological function recovery: The corner turning test was used to assess sensorimotor asymmetry. On postoperative day 7, the leftward turning deviation rate was 72.3%±6.8% in the percutaneous puncture group and 74.1%±7.5% in the traditional Longa group, with no statistically significant difference between the two groups (P>0.05). On postoperative day 28, the deviation rates decreased to 61.2%±5.4% and 67.8%±6.9% in the two groups, respectively (P<0.05), indicating that the percutaneous puncture group showed better recovery than the traditional Longa group. The beam walking test was used to assess motor coordination. On postoperative day 14, the average time to cross a 2 cm wide beam was 8.3±2.1 s in the percutaneous puncture group and 12.6±3.4 s in the traditional Longa group (P<0.01). The faster crossing speed in the percutaneous puncture group was attributed to faster recovery of physical strength due to normal postoperative eating function. Sensory neglect was assessed using the adhesive strip removal test. Small adhesive strips (0.3 cm × 0.4 cm) were attached to the palmar surface of both forepaws of rats, and the time it took for the rats to perceive and attempt to remove the strips on the affected side was recorded. On postoperative day 7, the sensory latency in the percutaneous puncture group was 35.6 ± 8.3 s, while that in the conventional Longa group was 38.2 ± 9.7 s, with no statistically significant difference between the two groups (P>0.05). On postoperative day 28, the latency in the percutaneous puncture group shortened to 12.4 ± 3.8 s, while that in the conventional Longa group was 19.7 ± 5.2 s (P<0.01), indicating that sensory function recovery in the percutaneous puncture group was superior to that in the conventional method group during long-term follow-up.

[0053] Evaluation of long-term healing at puncture site 20: Rats were sacrificed 28 days post-surgery, and the puncture segment of the common carotid artery at puncture site 16 was harvested for histological examination. HE staining showed complete repair of the vessel wall at puncture site 20, with a smooth and continuous intima, regular arrangement of the smooth muscle layer in the media, and no fibrosis or hyperplasia of the adventitia connective tissue. Verhoeff-Van Gieson elastic fiber staining confirmed the integrity of the elastic fibers at puncture site 20, without breakage or disorder. Immunofluorescence staining detected the expression of endothelial marker CD31 and smooth muscle marker α-SMA. The coverage rate of CD31-positive endothelial cells in the puncture site 20 area was 98.2% ± 1.3%, and the proportion of α-SMA-positive smooth muscle cells was 45.6% ± 3.8%. Both indicators showed no significant difference from the adjacent normal vessel wall (P>0.05), indicating that the minor vascular wall damage caused by the 30G puncture needle 1 achieved complete histological repair within 28 days. Doppler ultrasound examination of the common carotid artery at puncture point 20 showed an intraluminal diameter of 1.08±0.06 mm, with no significant stenosis compared to the preoperative baseline value (1.10±0.05 mm) (luminal narrowing rate less than 2%). Peak flow velocity and resistance index were both within the normal range. The long-term safety data showing no thrombosis or intimal hyperplasia at puncture point 20 further validated the reliability of the external pressure micro-balloon ring 12 hemostasis strategy. Compared to the blind end stump resulting from permanent ligation of the external carotid artery at puncture point 18 in traditional methods, the puncture-hemostasis-repair process of this invention relies entirely on the physiological repair capacity of the vessel wall, avoiding foreign body (suture) residue and chronic inflammatory reactions. Histopathological studies have confirmed the long-term safety and biocompatibility of this technical approach.

[0054] Model repeatability evaluation: Key parameters of 40 percutaneous MCAO models (90 min ischemia) prepared consecutively by the same operator were statistically analyzed. The puncture success rate was 92.5% (37 / 40), the embolization success rate (defined as a decrease in cortical blood flow to less than 20% of baseline as monitored by laser Doppler) was 94.6% (35 / 37), the 24 h postoperative survival rate was 97.1% (34 / 35), and the effective model rate after excluding subarachnoid hemorrhage was 91.4% (32 / 35). The coefficient of variation (CV) of infarct volume was 15.3%, which was superior to the CV values ​​(18% to 25%) reported in the literature for the traditional Longa method. Model learning curve analysis showed that the puncture success rate stabilized above 90% and the operation time stabilized at 12 to 15 min after the operator completed training with the first 10 rats, indicating that the learning difficulty of this technique is moderate and can be mastered after a short period of training.

[0055] Comprehensive Mechanism Analysis: The core innovation of this invention lies in miniaturizing the basic principles of the clinical Seldinger percutaneous puncture technique and applying them to the construction of an experimental animal model of cerebral ischemia. The percutaneous puncture approach fundamentally eliminates the need for the traditional suture occlusion method, which requires cutting and exposing blood vessels and ligating the external carotid artery 18. This ensures complete preservation of the anatomical integrity and blood flow of the three vessels—the common carotid artery 16, external carotid artery 18, and internal carotid artery 17—postoperatively. This change has a three-tiered progressive impact on the experimental model. In the first layer, the surgical injury level, percutaneous puncture causes only one 30G needle-sized puncture wound on the skin and one on the vessel wall, with a total damage area not exceeding 0.1 mm. 2 The tissue damage area is significantly smaller than that caused by the 3 to 4 cm incision of traditional methods, which results in hundreds of square millimeters of tissue damage. Postoperative inflammatory response and stress hormone levels are significantly reduced. In the second layer, namely the collateral circulation layer, the blood flow pathway of the external carotid artery 18 and all its branches (occipital artery, superior thyroid artery, lingual artery, facial artery, and superficial temporal artery) is completely preserved. This not only avoids direct ischemic damage to the temporal facial blood supply area, but more importantly, it preserves the ability of the external carotid artery 18 to provide collateral blood supply to the intracranial cavity through the ophthalmic artery anastomosis and the middle meningeal artery. This changes the reperfusion mode of the model from the single-source compensation of the Willis circle in the traditional method to a dual-pathway reperfusion of Willis circle compensation plus collateral supplementation of the external carotid artery 18. The latter is closer to the physiological reperfusion process of the internal carotid artery 17 after endovascular thrombectomy in patients with large vessel occlusion. At the third level, namely the quality of experimental data, eliminating ischemic complications in the external carotid artery 18 supply area means that confounding factors such as postoperative weight loss, eating disorders, and deviations in motor scores are systematically excluded. This allows neurobehavioral scores and brain histology results to more accurately reflect the severity and recovery process of cerebral ischemia injury itself, rather than the cumulative effect of surgical side effects.

[0056] The external pressure micro-balloon ring 12 hemostasis mechanism utilizes the natural hemostasis physiological processes of elastic recoil of vascular smooth muscle and platelet aggregation. The external pressure provided by the balloon serves only as an auxiliary means to accelerate the completion of the hemostasis process, avoiding the permanent vascular occlusion caused by suturing or ligation in traditional methods. The molecular basis of this hemostasis mechanism lies in the fact that the subendothelial collagen fibers exposed at the edge of the puncture needle tract trigger the binding of the platelet surface glycoprotein GPIb-IX-V complex to von Willebrand factor, activating the fibrinogen bridging aggregation reaction mediated by platelet integrin GPIIb / IIIa. At the same time, the myosin-actin contractile device in the vascular smooth muscle cells contracts under the stimulation of local injury signals. The synergistic effect of the two mechanisms enables the 0.31 mm diameter needle tract created by the 30G puncture needle 1 to be completely closed within 3 to 5 minutes. Furthermore, the puncture needle diameter (0.31 mm) is much smaller than the diameter of the rat common carotid artery (1.0 to 1.2 mm). The elastic recovery force of the annular elastic fiber and collagen fiber network of the vessel wall acts tangentially on the edge of the needle tract, generating a centripetal contraction tendency. This physical closure mechanism, combined with the platelet biological hemostasis mechanism, provides dual protection. The long-term histological results of Example 5 confirm that this minimally invasive hemostasis strategy is not only effective in the acute phase but also leaves no abnormalities in the long-term vessel wall structure.

[0057] The coaxial three-layer nested puncture and insertion device achieves seamless integration of three functional stages: puncture to establish access, microcatheter sheath 4 to maintain access, and suture delivery to complete embolization. The optimized size matching of each component ensures smooth operation and safety. A radial gap of 0.05 mm is reserved between the outer diameter of the puncture needle 1 (0.31 mm) and the outer diameter of the microcatheter sheath 4 (0.26 mm). This gap ensures that the microcatheter sheath 4 can slide freely in the needle lumen while preventing blood backflow during needle withdrawal due to excessive gap. A slight interference fit is formed between the inner diameter of the microcatheter sheath 4 (0.20 mm) and the outer diameter of the coated suture head (0.21 mm). The silicone coating 10 of the suture head 9 is slightly radially compressed within the lumen of the microcatheter sheath 4. After exiting the sheath and entering the blood vessel lumen, it returns to its original size, thus achieving good sealing between the suture head and the wall of the initial segment of the middle cerebral artery 19.

[0058] Model efficacy verification experiments show that, while maintaining a similar infarct volume and degree of neurological deficit as traditional methods, percutaneous puncture completely eliminates ischemic complications in the external carotid artery 18 supply area, significantly improves the postoperative weight recovery speed, and makes the cerebral blood flow recovery pattern during the reperfusion phase closer to the physiological reperfusion of clinical large vessel occlusion patients after thrombectomy, thereby improving the clinical translational reference value of the model.

[0059] The embodiments of the present invention are not limited to the specific embodiments described above. Those skilled in the art can make various equivalent changes or substitutions based on the technical solutions of the present invention, and all such changes or substitutions should be included within the protection scope of the present invention.

Claims

1. A method for percutaneous suture insertion in a cerebral ischemia model, characterized in that, Includes the following steps: S1. The experimental animals were anesthetized and fixed in a supine position. The neck skin was prepared and disinfected. S2. Under the guidance of a stereomicroscope, the common carotid artery is directly punctured percutaneously using an ultra-fine puncture needle. The puncture site is located 1 to 3 mm proximal to the bifurcation of the common carotid artery. The puncture needle is inserted into the anterior wall of the common carotid artery at an insertion angle of 15° to 30°. Blood return is observed at the tail end of the puncture needle to confirm that the needle tip has entered the lumen of the blood vessel. S3, the microcatheter sheath is inserted into the common carotid artery lumen through the needle lumen of the puncture needle, and then the puncture needle is withdrawn while the microcatheter sheath is retained; S4. After the puncture needle is withdrawn, place the external pressure micro-balloon ring on the skin surface corresponding to the puncture point, and inflate the external pressure micro-balloon ring to 30 to 50 mmHg to apply local pressure to stop bleeding at the puncture point on the anterior wall of the common carotid artery. S5, the suture embolism is pushed through the lumen of the microcatheter sheath, and the suture embolism is completed at the origin of the middle cerebral artery along the common carotid artery-internal carotid artery path; S6. After the embolization is maintained for the predetermined ischemic time, the embolus is withdrawn through the same microcatheter sheath to achieve reperfusion. After reperfusion is completed, the microcatheter sheath is withdrawn and the external pressure micro-balloon ring is used again to compress and stop the bleeding.

2. The percutaneous suture insertion method for a cerebral ischemia model according to claim 1, characterized in that, In step S2, the ultrafine puncture needle has a specification of 30G, an outer diameter of 0.31 mm, and a needle tip that is ground to a 12° to 18° bevel.

3. The percutaneous suture embolization method for a cerebral ischemia model according to claim 1, characterized in that, In step S3, the outer diameter of the microcatheter sheath is 0.24 to 0.28 mm, the wall thickness is 0.02 to 0.04 mm, and the length is 25 to 35 mm. The material of the microcatheter sheath is polyimide or polyetheretherketone.

4. The percutaneous suture embolization method for a cerebral ischemia model according to claim 1, characterized in that, In step S4, the inner diameter of the annular silicone airbag of the external pressure micro airbag ring is 1.5 to 2.5 mm and the outer diameter is 4 to 6 mm. After inflation, the pressure area generated locally at the puncture point covers the puncture needle track and its surrounding area within a range of 0.5 to 1.0 mm, and the pressure duration is 3 to 5 minutes.

5. The percutaneous suture insertion method for a cerebral ischemia model according to claim 1, characterized in that, In step S5, the suture is a silicone-coated nylon suture, the length of the coated section of the suture head is 4 to 6 mm, the outer diameter of the suture head after coating is 0.20 to 0.23 mm, and the insertion depth of the suture along the common carotid artery-internal carotid artery path is 17 to 20 mm.

6. A percutaneous suture insertion device for a cerebral ischemia model, characterized in that, include: An ultra-fine puncture needle, the tip of which is ground into a bevel structure, is used for percutaneous puncture of the common carotid artery; A microcatheter sheath, the outer diameter of which is smaller than the inner diameter of the ultra-fine puncture needle, is used to be inserted into the common carotid artery lumen through the puncture needle lumen and to serve as a suture embolus delivery channel. A plug pusher wire is provided, the outer diameter of which is smaller than the inner diameter of the microcatheter sheath, and the front end of the plug pusher wire is connected to a plug head coated with silicone. An external pressure micro-inflator ring, comprising an annular silicone inflator body and an inflation tubing and a micro-injector connected to the annular silicone inflator body, wherein the annular silicone inflator body is used to be fitted onto the skin surface corresponding to the puncture point and to implement local pressure hemostasis by inflation. The ultra-fine puncture needle, microcatheter sheath, and suture pusher core wire form a coaxial three-layer nested structure.

7. The percutaneous suture insertion device for a cerebral ischemia model according to claim 6, characterized in that, The ultrafine puncture needle has the following specifications: 30G, outer diameter of 0.31 mm, inner diameter of 0.16 to 0.18 mm, needle tip bevel angle of 12° to 18°, and needle body length of 15 to 25 mm.

8. The percutaneous suture insertion device for a cerebral ischemia model according to claim 6, characterized in that, The microcatheter sheath has an outer diameter of 0.24 to 0.28 mm, an inner diameter of 0.18 to 0.22 mm, a wall thickness of 0.02 to 0.04 mm, and a length of 25 to 35 mm. The distal end of the microcatheter sheath has a tapered transition section of 2° to 5° to reduce resistance when inserted into the vascular lumen.

9. The percutaneous suture insertion device for a cerebral ischemia model according to claim 6, characterized in that, The inner diameter of the annular silicone airbag body is 1.5 to 2.5 mm, the outer diameter is 4 to 6 mm, and the wall thickness is 0.3 to 0.5 mm. The inner diameter of the inflation tubing is 0.3 to 0.5 mm. The volume of the micro-injector is 0.1 to 0.5 mL. The working pressure range of the external pressure micro-airbag ring is 30 to 50 mmHg.

10. The percutaneous suture insertion device for a cerebral ischemia model according to claim 6, characterized in that, The outer diameter of the suture pusher wire is 0.10 to 0.14 mm, and the material is nickel-titanium alloy or stainless steel. The distal end of the suture pusher wire is provided with a flexible transition section with a length of 3 to 5 mm, which is used to provide flexibility when the suture passes through the curved section of the internal carotid artery.

Images