A system for detecting neuroinflammatory factors in sevoflurane-induced brain protection
Patent Information
- Application Number
- CN202611020644.6
- Authority / Receiving Office
- CN · China
- Patent Type
- Applications(China)
- Current Assignee / Owner
- Filing Date
- 2026-07-09
- Publication Date
- 2026-09-25
AI Technical Summary
[0004]为了解决系统容易将因血管硬化导致的冲刷效率下降错误地判定为神经炎症因子的主动生成，从而发出虚假的毒性预警，神经炎症因子检测效果较差的技术问题，本发明的目的在于提供一种七氟烷诱导脑保护中神经炎症因子检测系统，所采用的技术方案具体如下：
本发明根据不同时刻的呼气末七氟烷浓度分布，获得每次生化时间周期的累积血管舒张驱动量以及峰值给药速率，用于表征线性流体冲刷潜力以及触发血管硬化判定；根据不同生化时间周期的响应电流分布，获得每次生化时间周期的观测流体冲刷量，表征实际发生的浓度下降程度；根据初始血管顺应性系数、每次生化时间周期的观测流体冲刷量、累积血管舒张驱动量以及峰值给药速率，获得每次生化时间周期的神经炎症因子合成电流，反映理论冲刷量与观测冲刷量的残差，表征净生化合成量；根据不同生化时间周期的神经炎症因子合成电流分布，获得每次生化时间周期的累积神经毒性负荷，反映了受试者大脑承受的免疫炎症压力；对神经炎症进行检测。本发明通过准确获得累积神经毒性负荷，消除虚假毒性预警，提高神经炎症因子检测效果。
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Abstract
Description
Technical Field
[0001] This invention relates to the field of detection technology utilizing the chemical properties of sevoflurane, specifically to a detection system for neuroinflammatory factors in sevoflurane-induced brain protection. Background Technology
[0002] Sevoflurane causes cerebral vasodilation by activating vascular smooth muscle cell channels, increasing cerebral blood flow and accelerating interstitial fluid convection and metabolite clearance; and long-term or high-concentration exposure may induce microglial cell activation, leading to the synthesis and release of neuroinflammatory factors in the cerebral interstitial fluid.
[0003] In existing technologies, the detection of neuroinflammatory factors is based on the assumption of linear fluid dynamics, which assumes that the clearance efficiency of interstitial fluid is in a fixed proportion to the drug concentration or the degree of vasodilation. However, as biological soft tissue, the cerebral blood vessel wall has significant viscoelastic characteristics. When the concentration of sevoflurane increases sharply during the induction period, the blood vessel wall will exhibit stress hardening, causing the actual expansion rate of the blood vessel diameter to lag nonlinearly behind the rate of change of drug concentration. The system is prone to mistakenly identifying the decrease in flushing efficiency caused by vasodilation as the active generation of neuroinflammatory factors, thus issuing false toxicity warnings and resulting in poor neuroinflammatory detection. Summary of the Invention
[0004] To address the technical problem that systems often mistakenly interpret decreased flushing efficiency due to arteriosclerosis as the active generation of neuroinflammatory factors, thus issuing false toxicity warnings and resulting in poor detection of neuroinflammatory factors, the present invention aims to provide a sevoflurane-induced neuroinflammatory factor detection system. The specific technical solution adopted is as follows: This invention proposes a detection system for neuroinflammatory factors in sevoflurane-induced brain protection, the system comprising: The data acquisition module is used to acquire the end-tidal sevoflurane concentration at each moment and the response current for each biochemical time cycle. The vascular rheological feature extraction module is used to obtain the drug administration rate at each time point based on the end-tidal sevoflurane concentration distribution at different times; to obtain the cumulative vasodilatory driving force and peak drug administration rate for each biochemical time cycle based on the changing trend of the drug administration rate at different times of each biochemical time cycle; and to obtain the observed fluid flushing volume for each biochemical time cycle based on the response current distribution for different biochemical time cycles. The neuroinflammation quantification module is used to obtain the neuroinflammation factor synthesis current for each biochemical time cycle based on the initial vascular compliance coefficient, the observed fluid flushing volume for each biochemical time cycle, the cumulative vasodilation driving volume, and the peak drug administration rate; and to obtain the cumulative neurotoxicity load for each biochemical time cycle based on the distribution of neuroinflammation factor synthesis current for different biochemical time cycles. The inflammation detection module is used to detect neuroinflammation based on the cumulative neurotoxicity load over the latest biochemical time period.
[0005] Furthermore, the method for obtaining the drug administration rate includes: The difference in end-tidal sevoflurane concentration between each time point and the previous time point is taken as the dosing rate at each time point.
[0006] Furthermore, the method for obtaining the cumulative vasodilatory driving force and peak dosing rate includes: In each biochemical time cycle, the values of positive dosing rates at all times are summed up to obtain the cumulative vasodilatory driving force for each biochemical time cycle. The maximum dosing rate at all times within each biochemical time cycle is obtained as the peak dosing rate for each biochemical time cycle.
[0007] Furthermore, the method for obtaining the observed fluid scour volume includes: The difference between the response current of the previous biochemical time cycle and each biochemical time cycle is obtained as the observed fluid flushing amount for each biochemical time cycle.
[0008] Furthermore, the method for obtaining the neuroinflammatory factor synthesis current includes: The theoretical hemodynamic flushing volume for each biochemical time cycle is obtained based on the initial vascular compliance coefficient, the observed fluid flushing volume for each biochemical time cycle, the cumulative vasodilatory drive volume, and the peak drug administration rate. The difference between the theoretical hemodynamic flushing volume and the observed fluid flushing volume for each biochemical time cycle is obtained and used as the neuroinflammatory factor synthesis current for each biochemical time cycle.
[0009] Furthermore, the method for obtaining the theoretical hemodynamic flushing volume includes: The updated vascular compliance coefficient for each biochemical time cycle is obtained based on the initial vascular compliance coefficient, the observed fluid flushing volume for each biochemical time cycle, and the cumulative vascular dilation drive volume. Based on the peak dosing rate of each biochemical time cycle, the vascular stress sclerosis attenuation factor for each biochemical time cycle was obtained. The product of the cumulative vasodilatory drive, vascular stress attenuation factor, and updated vascular compliance coefficient for each biochemical time cycle is obtained as the theoretical hemodynamic flushing amount for each biochemical time cycle.
[0010] Furthermore, the method for obtaining the updated vascular compliance coefficient includes: If the peak dosing rate of each biochemical time cycle is less than the preset laminar flow linear threshold and the cumulative vasodilatory driving amount is greater than the preset minimum effective driving threshold, the ratio of the observed fluid flushing amount to the cumulative vasodilatory driving amount is obtained as the first ratio. Obtain the product of the preset update weight factor and the first ratio as the first product; obtain the difference between the positive integer 1 and the preset update weight factor, calculate the product of the difference result and the initial vascular compliance coefficient as the second product; obtain the sum of the first product and the second product as the updated vascular compliance coefficient. Conversely, the initial vascular compliance coefficient is used as the updated vascular compliance coefficient.
[0011] Furthermore, the method for obtaining the vascular stress-hardening attenuation factor includes: The product of the square of the peak dosing rate and the preset viscoelastic constant of the blood vessel wall is obtained. The sum of the positive integer 1 and the product is then negatively correlated and mapped as the vascular stress hardening attenuation factor for each biochemical time cycle.
[0012] Furthermore, the method for obtaining the cumulative neurotoxic load includes: The difference between the neuroinflammatory factor synthesis current and the preset sensor detection limit is calculated for each biochemical time cycle. The maximum value between the difference result and the preset difference threshold is selected as the effective inflammation generation rate for each biochemical time cycle.
[0013] The cumulative value of the effective inflammation generation rate of all biochemical time cycles within the neighborhood of each biochemical time cycle is obtained as the cumulative neurotoxicity load for each biochemical time cycle.
[0014] Furthermore, the detection of neuroinflammation includes: If the cumulative neurotoxicity load of each biochemical time cycle exceeds the preset safety threshold for brain nerve damage, an early warning for neuroinflammation will be issued.
[0015] The present invention has the following beneficial effects: This invention obtains the cumulative vasodilatory driving force and peak dosing rate for each biochemical time cycle based on the end-tidal sevoflurane concentration distribution at different times, used to characterize the linear fluid flushing potential and determine the triggering of arteriosclerosis; it obtains the observed fluid flushing volume for each biochemical time cycle based on the response current distribution for different biochemical time cycles, characterizing the actual concentration decrease; it obtains the neuroinflammatory factor synthesis current for each biochemical time cycle based on the initial vascular compliance coefficient, the observed fluid flushing volume for each biochemical time cycle, the cumulative vasodilatory driving force, and the peak dosing rate, reflecting the residual between the theoretical flushing volume and the observed flushing volume, characterizing the net biochemical synthesis volume; it obtains the cumulative neurotoxicity load for each biochemical time cycle based on the neuroinflammatory factor synthesis current distribution for different biochemical time cycles, reflecting the immune inflammatory pressure on the subject's brain; and it detects neuroinflammation. This invention, by accurately obtaining the cumulative neurotoxicity load, eliminates false toxicity warnings and improves the detection effect of neuroinflammatory factors. Attached Figure Description
[0016] Figure 1 This is a structural block diagram of a sevoflurane-induced neuroinflammatory factor detection system according to an embodiment of the present invention; Figure 2 The flowchart illustrates a method for obtaining theoretical hemodynamic flushing volume according to an embodiment of the present invention. Detailed Implementation
[0017] Unless otherwise defined, all technical and scientific terms used herein have the same meaning as commonly understood by one of ordinary skill in the art to which this invention pertains.
[0018] The following describes in detail, with reference to the accompanying drawings, a specific scheme for the detection system of neuroinflammatory factors in sevoflurane-induced brain protection provided by the present invention.
[0019] Please see Figure 1 The diagram illustrates a structural block diagram of a sevoflurane-induced neuroinflammatory factor detection system according to an embodiment of the present invention. The system specifically includes: a data acquisition module 101, a vascular rheological feature extraction module 102, a neuroinflammatory quantification module 103, and an inflammation detection module 104. The data acquisition module 101 is used to acquire the end-tidal sevoflurane concentration at each moment and the response current for each biochemical time cycle.
[0020] In an embodiment of the present invention, during the anesthesia induction period, rapid drug administration can induce stress hardening of the vascular wall, causing the actual increase in blood flow to lag behind the linear expectation. This lag is reflected in the monitoring data as a smaller-than-expected decrease in interstitial fluid concentration, leading to the erroneous attribution of this concentration residue caused by physical lag to the new generation of neuroinflammatory factors. Therefore, the changes in the drug administration rate are reflected by analyzing the sevoflurane concentration at different times. First, considering that the vasomotor state of the brain is directly driven by the rate of change of the partial pressure of sevoflurane in the blood, and that the gas concentration signal collected through the breathing circuit contains physiological fluctuations in respiratory rate, direct use would lead to computational noise. The processor reads the end-tidal sevoflurane concentration output by the anesthesia machine in real time through a digital interface at a preset sampling frequency.
[0021] It should be noted that, in one embodiment of the present invention, the preset sampling frequency is 1Hz, that is, the time interval is 1 second; in other embodiments of the present invention, the magnitude of the preset sampling frequency can be set according to the specific situation, and will not be limited or described in detail here.
[0022] In addition, the processor receives the current signal sent by the microneedle electrochemical sensor implanted in the subject's cerebral cortex. The sensor completes a biochemical scan every fixed period and outputs a discrete biochemical sensor response current for subsequent analysis. It should be noted that in the embodiments of the present invention, the fixed period is set by the implementer according to the specific situation, such as 300 seconds, and is not limited or described here.
[0023] It should be noted that, in order to facilitate subsequent data processing, a moving average filtering algorithm was used to filter out respiratory ripples and obtain a smoothed end-tidal sevoflurane concentration for subsequent analysis; the specific methods are well known to those skilled in the art and will not be described in detail here.
[0024] The vascular rheological feature extraction module 102 is used to obtain the drug administration rate at each moment based on the end-tidal sevoflurane concentration distribution at different times; to obtain the cumulative vasodilatory driving force and peak drug administration rate for each biochemical time cycle based on the changing trend of the drug administration rate at different times of each biochemical time cycle; and to obtain the observed fluid flushing volume for each biochemical time cycle based on the response current distribution for different biochemical time cycles.
[0025] End-tidal sevoflurane concentration is a direct indicator of the depth of anesthesia, quantifying the instantaneous mechanical stress exerted on the blood vessel wall by changes in drug concentration; and the dosing rate at each moment is obtained based on the distribution of end-tidal sevoflurane concentration at different times.
[0026] Preferably, in one embodiment of the present invention, the method for obtaining the drug administration rate includes: The difference in end-tidal sevoflurane concentration between each time point and the previous time point is taken as the dosing rate at each time point.
[0027] Based on this, the difference between time points represents the absolute value of the difference between time points, and the drug administration rate reflects the intensity of the regulation of the depth of anesthesia. The higher the drug administration rate, the deeper the anesthesia characteristics and the more vasodilates. The lower the drug administration rate, the more negative the change, the shallower the anesthesia and the more vasoconstricts.
[0028] Based on the ideal elastomer assumption, it is believed that the degree of cerebral vasodilation is linearly positively correlated with the concentration of anesthetic drugs; the dosing rate reflects the intensity of the regulation of anesthesia depth. The higher the dosing rate, the deeper the anesthesia and the more the blood vessels tend to dilate; the lower the dosing rate, the shallower the anesthesia and the more the blood vessels tend to constrict. Therefore, based on the trend of dosing rate changes, the vasodilation status and dosing status are quantified; according to the trend of dosing rate changes at different times in each biochemical time cycle, the cumulative vasodilation driving force and peak dosing rate of each biochemical time cycle are obtained.
[0029] Preferably, in one embodiment of the present invention, the method for obtaining the cumulative vasodilatory driving force and the peak drug delivery rate includes: In each biochemical time cycle, the values of positive dosing rates at all times are summed up to obtain the cumulative vasodilatory driving force for each biochemical time cycle. The maximum dosing rate at all times within each biochemical time cycle is obtained as the peak dosing rate for each biochemical time cycle.
[0030] Because the physical flushing effect leads to a decrease in the concentration of metabolites in the interstitial fluid and a decrease in current, while the synthesis caused by neuroinflammatory reactions leads to an increase in concentration and an increase in current, the flushing amount is quantified by analyzing the distribution of the response current. Based on the distribution of the response current in different biochemical time periods, the observed fluid flushing amount for each biochemical time period is obtained.
[0031] Preferably, in one embodiment of the present invention, the method for obtaining the fluid scour volume includes: The difference between the response current of the previous biochemical time cycle and each biochemical time cycle is obtained as the observed fluid flushing amount for each biochemical time cycle.
[0032] Based on this, the larger the observed fluid scouring volume, the larger the response current of the previous biochemical time cycle, the current shows a downward trend, and the greater the physical scouring effect; the smaller the observed fluid scouring volume, the smaller the response current of the previous biochemical time cycle relative to the subsequent one, the current shows an upward trend, the biochemical synthesis effect exceeds the physical removal, and the greater the neuroinflammatory synthesis.
[0033] The neuroinflammation quantification module 103 is used to obtain the neuroinflammation factor synthesis current for each biochemical time cycle based on the initial vascular compliance coefficient, the observed fluid flushing volume for each biochemical time cycle, the cumulative vasodilation driving volume, and the peak drug administration rate; and to obtain the cumulative neurotoxicity load for each biochemical time cycle based on the distribution of neuroinflammation factor synthesis current for different biochemical time cycles.
[0034] As biological soft tissue, the cerebral blood vessel wall has significant viscoelastic characteristics. During the induction period when the concentration of sevoflurane changes drastically, the blood vessel wall will exhibit stress hardening, causing the actual vasodilation amplitude to lag nonlinearly behind the change in drug concentration. Therefore, the neuroinflammatory factor synthesis current in each biochemical time cycle can be obtained based on the initial vascular compliance coefficient, the observed fluid flushing volume in each biochemical time cycle, the cumulative vasodilatory driving volume, and the peak drug administration rate.
[0035] Preferably, in one embodiment of the present invention, the method for obtaining the synthetic current of neuroinflammatory factors includes: The first step is to obtain the theoretical hemodynamic flushing volume for each biochemical time cycle based on the initial vascular compliance coefficient, the observed fluid flushing volume for each biochemical time cycle, the cumulative vasodilatory drive volume, and the peak drug administration rate.
[0036] It should be noted that the initial vascular compliance coefficient characterizes the theoretical proportion of the observed fluid flushing caused by a unit cumulative vascular dilation driving force under ideal laminar flow conditions and without vascular sclerosis. In the embodiments of the present invention, in the initial stage of the system, the processor retrieves the population mean obtained from the memory based on the statistics of a large clinical sample as the initial vascular compliance coefficient. The larger the initial vascular compliance coefficient, the more the blood vessels are expected to dilate under the same driving force, the more interstitial fluid is theoretically flushed away, and the greater the theoretical hemodynamic flushing. The observed fluid flushing volume reflects the actual measured decrease in interstitial fluid concentration. When the observed fluid flushing volume is negative, the current increases, indicating that the amount of biochemical synthesis exceeds the amount of physical flushing. The cumulative vasodilation driving force reflects the total potential energy driving the flow of interstitial fluid when the blood vessel is an ideal elastic body. The greater the cumulative vasodilation driving force, the greater the theoretical hemodynamic flushing volume. Peak dosing rate reflects the rate of the most drastic single dosing operation. The higher the rate, the greater the likelihood that the blood vessels will enter a nonlinear sclerotic state, and the smaller the theoretical hemodynamic flushing volume.
[0037] Preferably, in one embodiment of the present invention, the method for obtaining the theoretical hemodynamic flushing volume is described in [reference needed]. Figure 2 It illustrates a flowchart of a method for obtaining theoretical hemodynamic flushing volume, including: Step S201: Based on the initial vascular compliance coefficient, the observed fluid flushing volume for each biochemical time cycle, and the cumulative vascular dilation driving volume, obtain the updated vascular compliance coefficient for each biochemical time cycle.
[0038] Preferably, in one embodiment of the present invention, the method for obtaining the updated vascular compliance coefficient includes: If the peak dosing rate of each biochemical time cycle is less than the preset laminar flow linear threshold and the cumulative vasodilatory driving amount is greater than the preset minimum effective driving threshold, the ratio of the observed fluid flushing amount to the cumulative vasodilatory driving amount is obtained as the first ratio. It should be noted that, in one embodiment of the present invention, the preset laminar flow linearity threshold is set based on relevant historical experience. The preset minimum effective drive threshold is set to 5%-10% of the system's full-scale drive quantity. In other embodiments of the present invention, the preset laminar linear threshold and the minimum effective drive threshold can be set according to specific circumstances, and are not limited or elaborated here.
[0039] Obtain the product of the preset update weight factor and the first ratio as the first product; obtain the difference between the positive integer 1 and the preset update weight factor, calculate the product of the difference result and the initial vascular compliance coefficient as the second product; obtain the sum of the first product and the second product as the updated vascular compliance coefficient. It should be noted that the greater the observed fluid flushing volume is than the cumulative vasodilation driving volume, the larger the first ratio, the greater the physical flushing volume, the greater the initial vascular compliance coefficient, and the better the vascular compliance.
[0040] The formula is expressed as: ;in, This indicates the updated vascular compliance coefficient; This indicates the preset update weight factor; Indicates the initial vascular compliance coefficient; Indicates the first Observed fluid scouring volume during the secondary metastasis time period; Indicates the first The cumulative vasodilatory driving force over the secondary biochemical time cycle.
[0041] It should be noted that, in order to ensure gradual convergence to the subject's true vascular compliance benchmark and to filter out random errors from a single measurement, in one embodiment of the present invention, the preset update weighting factor is set to 0.1; in other embodiments of the present invention, the size of the preset update weighting factor can be set according to specific circumstances, and will not be limited or elaborated here.
[0042] Conversely, the initial vascular compliance coefficient is used as the updated vascular compliance coefficient. It should be noted that when performing the calculation for the next biochemical time period, the updated vascular compliance coefficient obtained in the current biochemical time period is used instead of the initial vascular compliance coefficient and substituted into the calculation.
[0043] Step S202: Based on the peak dosing rate of each biochemical time cycle, obtain the vascular stress sclerosis attenuation factor for each biochemical time cycle.
[0044] Peak dosing rate represents the maximum dosing rate within a cycle, reflecting the intensity of concentration regulation during the anesthesia induction period. The larger the maximum value, the greater the maximum instantaneous mechanical impact on the blood vessel wall, the more it enters the nonlinear hardening state, and the smaller the vascular stress hardening attenuation factor.
[0045] Preferably, in one embodiment of the present invention, the method for obtaining the vascular stress hardening attenuation factor includes: The product of the square of the peak dosing rate and the preset viscoelastic constant of the blood vessel wall is obtained. The sum of the positive integer 1 and the product is then negatively correlated and mapped as the vascular stress hardening attenuation factor for each biochemical time cycle.
[0046] Based on this, the higher the peak drug delivery rate, the more drastically the tissue stiffness increases, and the smaller the vascular stress hardening attenuation factor becomes, resulting in a nonlinear decay of physical flushing efficiency.
[0047] It should be noted that, in the embodiments of the present invention, the preset viscoelastic constant of the blood vessel wall is pre-stored in the system's database and can be automatically matched and called according to the subject's age range.
[0048] It should be noted that, in one embodiment of the present invention, negative correlation mapping is performed by taking the reciprocal; in other embodiments of the present invention, it can also be performed using an exponential function with the natural constant as the base. Negative correlation mapping is performed using techniques well-known to those skilled in the art, which will not be limited or elaborated upon here.
[0049] Step S203: Obtain the product of the cumulative vasodilatory drive, vascular stress attenuation factor, and updated vascular compliance coefficient for each biochemical time cycle, as the theoretical hemodynamic flushing amount for each biochemical time cycle.
[0050] Based on this, the larger the vascular compliance coefficient, the greater the physical flushing and the greater the theoretical hemodynamic flushing; the vascular stress hardening attenuation factor reflects that when the strain rate increases, the tissue stiffness rises sharply, hindering the next expansion. Therefore, the larger the vascular stress hardening attenuation factor, the smaller the tissue stiffness and the greater the theoretical hemodynamic flushing; the greater the cumulative vasodilation driving force, the greater the potential energy driving the interstitial fluid flow and the greater the flushing.
[0051] The second step is to obtain the difference between the theoretical hemodynamic flushing volume and the observed fluid flushing volume for each biochemical time cycle, which is used as the neuroinflammatory factor synthesis current for each biochemical time cycle.
[0052] By comparing the theoretical hemodynamic flushing volume with the observed fluid flushing volume, the net synthesis of neuroinflammatory factors masked by the physical dilution effect is reflected. The larger the difference, the greater the content of neuroinflammatory factors.
[0053] The current synthesized by neuroinflammatory factors reflects the net synthesis of neuroinflammatory factors masked by the physical dilution effect. A higher net synthesis indicates a greater likelihood of net neuroinflammatory factor generation, which helps quantify the cumulative neurotoxicity load. Based on the distribution of neuroinflammatory factor synthesis currents over different biochemical time periods, the cumulative neurotoxicity load for each biochemical time period was obtained.
[0054] Preferably, in one embodiment of the present invention, the method for obtaining the cumulative neurotoxicity load includes: The difference between the neuroinflammatory factor synthesis current and the preset sensor detection lower limit is calculated for each biochemical time cycle. The maximum value between the difference result and the preset difference threshold is selected as the effective inflammation generation rate for each biochemical time cycle. It should be noted that, in the embodiments of the present invention, the method for obtaining the preset sensor detection lower limit is: to preset it according to the signal-to-noise ratio characteristics calibrated by the sensor at the factory.
[0055] It should be noted that, in the embodiments of the present invention, in order to measure the deviation between the synthesis current of neuroinflammatory factors and the preset sensor detection lower limit, the preset difference threshold is set to 0.
[0056] The cumulative value of the effective inflammation generation rate of all biochemical time cycles within the neighborhood of each biochemical time cycle is obtained as the cumulative neurotoxicity load for each biochemical time cycle.
[0057] Based on this, cumulative neurotoxicity load represents the total amount of neuroinflammatory factors generated during the period induced by sevoflurane exposure that cannot be explained by blood flow flushing, reflecting the immune inflammatory stress experienced by the subject's brain.
[0058] It should be noted that, in one embodiment of the present invention, the method for obtaining the neighborhood range includes: taking each biochemical time cycle as a benchmark, selecting a range consisting of all cycles within a preset time range, wherein the preset time range is set to 30 minutes, that is, analyzing the biochemical time cycles obtained in the past 30 minutes. In other embodiments of the present invention, the size of the neighborhood range can be set according to specific circumstances, and is not limited or described here.
[0059] The inflammation detection module 104 is used to detect neuroinflammation based on the cumulative neurotoxicity load of the latest biochemical time period.
[0060] The cumulative neurotoxicity load reflects the immune inflammatory stress experienced by the subject's brain; the greater the cumulative neurotoxicity load, the greater the risk of neuroinflammation.
[0061] Preferably, in one embodiment of the present invention, detecting nerve inflammation includes: If the cumulative neurotoxicity load of each biochemical time cycle exceeds the preset safety threshold for brain nerve damage, an early warning for neuroinflammation will be issued.
[0062] It should be noted that, in the embodiments of the present invention, the method for obtaining the preset safety threshold for brain nerve injury is: the electrochemical equivalent calculated based on the median lethal cumulative dose of related inflammatory factors causing apoptosis of developing neurons.
[0063] Based on this, if the concentration exceeds the preset safety threshold for brain nerve damage, the accumulated risk of neuroinflammation exceeds the safety limit, requiring a reduction in drug concentration or the implementation of anti-inflammatory intervention to achieve real-time protection of brain function during sevoflurane anesthesia.
[0064] In summary, this invention obtains the cumulative vasodilatory driving force and peak dosing rate for each biochemical time cycle based on the end-tidal sevoflurane concentration distribution at different times; it obtains the observed fluid flushing volume for each biochemical time cycle based on the response current distribution for different biochemical time cycles; it obtains the neuroinflammatory factor synthesis current for each biochemical time cycle based on the initial vascular compliance coefficient, the observed fluid flushing volume for each biochemical time cycle, the cumulative vasodilatory driving force, and the peak dosing rate; and it obtains the cumulative neurotoxicity load for each biochemical time cycle based on the neuroinflammatory factor synthesis current distribution for different biochemical time cycles; and it detects neuroinflammation. This invention eliminates false toxicity warnings and improves the detection effect of neuroinflammatory factors by accurately obtaining the cumulative neurotoxicity load.
Claims
1. A detection system for neuroinflammatory factors in sevoflurane-induced brain protection, characterized in that, The system includes: The data acquisition module is used to acquire the end-tidal sevoflurane concentration at each moment and the response current for each biochemical time cycle. The vascular rheological feature extraction module is used to obtain the drug administration rate at each time point based on the end-tidal sevoflurane concentration distribution at different times; to obtain the cumulative vasodilatory driving force and peak drug administration rate for each biochemical time cycle based on the changing trend of the drug administration rate at different times of each biochemical time cycle; and to obtain the observed fluid flushing volume for each biochemical time cycle based on the response current distribution for different biochemical time cycles. The neuroinflammation quantification module is used to obtain the neuroinflammation factor synthesis current for each biochemical time cycle based on the initial vascular compliance coefficient, the observed fluid flushing volume for each biochemical time cycle, the cumulative vasodilation driving volume, and the peak drug administration rate; and to obtain the cumulative neurotoxicity load for each biochemical time cycle based on the distribution of neuroinflammation factor synthesis current for different biochemical time cycles. The inflammation detection module is used to detect neuroinflammation based on the cumulative neurotoxicity load over the latest biochemical time period.
2. The sevoflurane-induced neuroinflammatory factor detection system according to claim 1, characterized in that, The method for obtaining the drug administration rate includes: The difference in end-tidal sevoflurane concentration between each time point and the previous time point is taken as the dosing rate at each time point.
3. The sevoflurane-induced neuroinflammatory factor detection system according to claim 1, characterized in that, The methods for obtaining the cumulative vasodilatory driving force and peak dosing rate include: In each biochemical time cycle, the values of positive dosing rates at all times are summed up to obtain the cumulative vasodilatory driving force for each biochemical time cycle. The maximum dosing rate at all times within each biochemical time cycle is obtained as the peak dosing rate for each biochemical time cycle.
4. The sevoflurane-induced neuroinflammatory factor detection system according to claim 1, characterized in that, The method for obtaining the observed fluid scour volume includes: The difference between the response current of the previous biochemical time cycle and each biochemical time cycle is obtained as the observed fluid flushing amount for each biochemical time cycle.
5. The sevoflurane-induced neuroinflammatory factor detection system according to claim 1, characterized in that, The method for obtaining the neuroinflammatory factor synthesis current includes: The theoretical hemodynamic flushing volume for each biochemical time cycle is obtained based on the initial vascular compliance coefficient, the observed fluid flushing volume for each biochemical time cycle, the cumulative vasodilatory drive volume, and the peak drug administration rate. The difference between the theoretical hemodynamic flushing volume and the observed fluid flushing volume for each biochemical time cycle is obtained and used as the neuroinflammatory factor synthesis current for each biochemical time cycle.
6. The sevoflurane-induced neuroinflammatory factor detection system according to claim 5, characterized in that, The method for obtaining the theoretical hemodynamic flushing volume includes: The updated vascular compliance coefficient for each biochemical time cycle is obtained based on the initial vascular compliance coefficient, the observed fluid flushing volume for each biochemical time cycle, and the cumulative vascular dilation drive volume. Based on the peak dosing rate of each biochemical time cycle, the vascular stress sclerosis attenuation factor for each biochemical time cycle was obtained. The product of the cumulative vasodilatory drive, vascular stress attenuation factor, and updated vascular compliance coefficient for each biochemical time cycle is obtained as the theoretical hemodynamic flushing amount for each biochemical time cycle.
7. The sevoflurane-induced neuroinflammatory factor detection system according to claim 6, characterized in that, The method for obtaining the updated vascular compliance coefficient includes: If the peak dosing rate of each biochemical time cycle is less than the preset laminar flow linear threshold and the cumulative vasodilatory driving amount is greater than the preset minimum effective driving threshold, the ratio of the observed fluid flushing amount to the cumulative vasodilatory driving amount is obtained as the first ratio. Obtain the product of the preset update weight factor and the first ratio as the first product; obtain the difference between the positive integer 1 and the preset update weight factor, calculate the product of the difference result and the initial vascular compliance coefficient as the second product; obtain the sum of the first product and the second product as the updated vascular compliance coefficient. Conversely, the initial vascular compliance coefficient is used as the updated vascular compliance coefficient.
8. The sevoflurane-induced neuroinflammatory factor detection system according to claim 6, characterized in that, The method for obtaining the vascular stress-atrophy attenuation factor includes: The product of the square of the peak dosing rate and the preset viscoelastic constant of the blood vessel wall is obtained. The sum of the positive integer 1 and the product is then negatively correlated and mapped as the vascular stress hardening attenuation factor for each biochemical time cycle.
9. The sevoflurane-induced neuroinflammatory factor detection system according to claim 1, characterized in that, The method for obtaining the cumulative neurotoxic load includes: The difference between the neuroinflammatory factor synthesis current and the preset sensor detection lower limit is calculated for each biochemical time cycle. The maximum value between the difference result and the preset difference threshold is selected as the effective inflammation generation rate for each biochemical time cycle. The cumulative value of the effective inflammation generation rate of all biochemical time cycles within the neighborhood of each biochemical time cycle is obtained as the cumulative neurotoxicity load for each biochemical time cycle.
10. The detection system for neuroinflammatory factors in sevoflurane-induced brain protection according to claim 1, characterized in that, The detection of neuroinflammation includes: If the cumulative neurotoxicity load of each biochemical time cycle exceeds the preset safety threshold for brain nerve damage, an early warning for neuroinflammation will be issued.