Balloon controllable in in-vivo flow and capable of reducing ischemia reperfusion injury

Abstract

The invention provides a balloon controllable in in-vivo flow and capable of reducing ischemia reperfusion injury and relates to the field of intervention medical instruments. The balloon comprises atail-end joint, a hard pushing tube, a perfusion hose, a balloon body, a guide wire and a flow control part, and the flow control part is composed of an inner perfusion hole, a wrapping outer sheath and an inner perfusion hole mark. After the balloon is inflated, the far end of an infarction zone or an ischemia zone can be perfused accurately and slowly by sliding the wrapping outer sheath withoutreleasing the balloon so as to avoid the ischemia reperfusion injury; the balloon only needs to be expanded and released once while the far end is perfused, so that vascular injury, plaque shedding and no-reflow of blood vessels at the far end can be reduced or avoided.

Description

Technical field: [0001] The invention relates to the field of interventional medical devices, in particular to a balloon for reducing ischemia-reperfusion injury with controllable flow in the body used in acute vascular occlusion. Background technique: [0002] At present, acute vascular occlusive disease is the main cause of death in the Chinese population, including acute myocardial infarction, cerebral infarction, peripheral arterial vascular embolism, etc., patients with acute vascular occlusive disease, the preferred method is emergency interventional treatment to open the infarct-related blood vessels, and then Perfuse the infarcted area; however, in the process of emergency intervention, directly opening the occluded blood vessel will cause further damage, which is called ischemia-reperfusion injury, resulting in further damage to the organs in the infarcted area. [0003] Although the existing balloon perfusion equipment understands the ischemic injury, the specific ...

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Problems solved by technology

[0002] At present, acute vascular occlusive disease is the main cause of death in the Chinese population, including acute myocardial infarction, cerebral infarction, peripheral arterial vascular embolism, etc., patients with acute vascular occlusive disease, the preferred method is emergency interventional treatment to open the infarct-related blood vessels, and then Perfuse the infarcted area; however, during emergency interventional treatment, directly opening the occluded blood vessel will cause further damage, which is called ischemia-reperfusion injury, resulting in further damage to the organs in the infarcted area

[0003] Although the existing balloon perfusion equipment understands ischemic injury, the specific cause of the injury is not clear

At present, there is a postconditioning mode (ischemic postconditioning) to avoid ischemia-reperfusion injury. The specific operation method is to use the balloon to repeatedly expand and retract in the blood vessel, causing the blood flow in the blood vessel to pulse in an "all or nothing" manner. Intermittent recovery is the process of adapting the ischemic area to reperfusion. Animal experiments have proved that this post-conditioning mode can partially alleviate ischemia-reperfusion injury; however, this "all or nothing" pulsed blood flow recovery itself is It may lead to ischemia-reperfusion injury. At the same time, repeated expansion and retraction of the balloon may lead to thrombus and plaque shedding, causing and aggravating no-reflow; mostly negative

[0004] The traditional method of interventional therapy for acute vascular occlusive diseases is to use intravascular guide wires and balloons to quickly open the acutely occluded blood vessels. However, the applicant has found through a large number of animal experiments and clinical experiments that the blood flow of the occluded blood vessels is restored, and sudden reperfusion will occur. In the distal myocardium, the sudden recovery of energy and oxygen leads to a sudden change in the intracellular environment, a sudden imbalance in pH, etc., which causes severe contraction and damage to the membrane of edema cells, resulting in further necrosis of ischemic organs

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