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目的 :探讨大鼠脑缺血 -再灌注后脑组织微血管通透性的变化规律 ,为进一步探讨脑缺血及再灌注损伤机制提供参考数据。方法 :应用荧光素钠 (分子量 3 86 ,Fl Na)和 FITC标记的右旋糖苷( FD4,分子量 40 0 0 )为荧光示踪剂 ,以单侧颈总动脉远心端及同侧颈静脉插管并连接二管造成颈总动脉向颈静脉的引流 ,同时用动脉夹夹闭对侧颈总动脉造成脑缺血模型。缺血 1h后松开动脉夹并中断引流造成再灌注模型。测量脑组织荧光强度反映脑微血管通透性的变化。结果 :单纯的脑缺血即可引起脑组织微血管通透性的增强 ,再灌注后对小分子量物质的通透性随再灌注时间的延长有增加的趋势 ,而对较大分子量物质的通透性基本维持在同一水平。结论 :即使是在再灌注损伤最严重时 ,脑微血管对较大分子量的物质通透仍不明显 ,说明血 -脑屏障的存在可以有效地防止有害物质通过微血管壁侵入脑组织 ,但一旦进入脑组织 ,将滞留于脑组织中不易清除。
Objective: To investigate the changes of microvessel permeability after cerebral ischemia-reperfusion in rats and provide reference data for further exploring the mechanism of cerebral ischemia and reperfusion injury. Methods: Fluorescein sodium (molecular weight 386, Fl Na) and FITC-labeled dextran (FD4, molecular weight 40 000) were used as fluorescent tracer. The distal carotid artery Tube and connect the two tubes to cause the common carotid artery to the jugular vein drainage, while clamping the contralateral common carotid artery with cerebral artery occlusion caused by cerebral ischemia model. After 1h of ischemia, the artery clip was released and the drainage was interrupted to cause the reperfusion model. Measurement of brain tissue fluorescence intensity reflects changes in cerebral microvascular permeability. Results: Cerebral ischemia could induce the increase of microvessel permeability of brain tissue. The permeability of small molecular weight substances increased with the reperfusion time after reperfusion, while the permeation of larger molecular weight substances Sex basically maintained at the same level. Conclusion: Even in the most severe reperfusion injury, the cerebral microvascular permeability of larger molecular weight substances is still not obvious, indicating that the presence of blood-brain barrier can effectively prevent harmful substances through the microvascular wall invasion of brain tissue, but once into the brain Tissue, will stay in the brain tissue is not easy to remove.