缺血后处理神经保护作用的实验研究

目的：探讨缺血后处理对大鼠全脑缺血再灌注损伤的影响。方法30只雄性SD大鼠随机分为三组（n=10），建立四血管阻断全脑缺血模型。假手术组：单纯麻醉和手术操作，无缺血过程；缺血再灌注组：缺血10 min后再灌注；缺血后处理组：缺血10 min后以10 s再灌注/10 s阻断，共6个循环实现缺血后处理。再灌注后于第1天和第3天进行行为学观察；在72 h后进行病理学检测。结果 Morris水迷宫提示：再灌注后第1天，缺血再灌注组的平均上台时间（84.76±10.22）s较假手术组（27.08±7.52）s明显延长，差异有统计学意义（t=14.84， P＜0.05），缺血后处理组的平均上台时间（50.24±9.72）s明显少于缺血再灌注组，差异有统计学意义（t=7.74， P＜0.05）。再灌注后第3天，缺血再灌注组的上台时间（55.90±11.26）s仍明显长于缺血后处理组（29.22±5.82）s，差异有统计学意义（t=6.65， P＜0.05）。72 h后病理学染色提示：缺血再灌注组和缺血后处理组海马CA1区存活神经元分别为假手术组的25.90％和64.60％。结论缺血后处理可以明显减少大鼠全脑缺血再灌注后神经元死亡，减轻行为学缺损，对大鼠全脑缺血再灌注有神经保护作用。

Experimental research of neuroprotective effects of ischemic postconditioning

Objective To investigate the effect of ischemic postconditioning on global ischemia-reperfusion injury in rats. Methods Thirty male SD rats were randomly assigned to three groups with ten rats each and four blood vessel that blocking the whole cerebral ischemia model was set up. Sham group was just received anesthesia and operation without is-chemia. Ischemia-reperfusion group was received reperfusion at 10 minutes after ischemia. Ischemic postconditioning group was received reperfusion 10 seconds and blocking 10 seconds at 10 minutes after ischemia, thus circling 6 times. Behavior tests were observed at first and third day after reperfusion. Pathology detections were taken at 72 hours after reperfusion. Results Morris Water Maze showed that the latency to platform of ischemia-reperfusion group was（84.76±10.22） seconds which was significantly longer than sham group that was （27.08±7.52） seconds （t=14.84, P＆lt;0.05） as well as ischemic postconditioning group that was（50.24±9.72） seconds（t=7.74, P＆lt;0.05） at first day after reperfusion. The latency to plat-form of ischemia-reperfusion group was（55.90±11.26） seconds which was significantly longer than ischemic postcondition-ing group that was（29.22±5.82）seconds at third day after reperfusion（t=6.65, P＆lt;0.05）.The pathologic results showed that the neuron survival rate of ischemia-reperfusion group and ischemic postconditioning group were 25.90% and 64.60%. Conclusion Ischemia postconditioning could reduce the brain neuron death after ischemia reperfusion in rats, attenuate behavioral defects and has neuroprotection on ischemia-reperfusion in rats.