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目的用复制的大鼠急性脑缺血－再灌注动物模型，观察脑内生化代谢、水含量及病理组织学方面的变化，并观察新型钙通道阻滞剂氨氯地平对上述指标的影响，及对脑缺血－再灌注的影响。方法雄性Ｗｉｓｔａｒ大鼠，采用改良的Ｐｕｌｓｉｎｅｌｉ的四血管闭塞法制备动物模型，除假手术组外均行双侧椎动脉凝闭及双侧颈总动脉夹闭，再灌注时开放动脉夹再通。过氧化脂质含量测定采用Ｔｓｕｃｈｉｄａ的ＷＳＰＳ法，超氧化物歧化酶活性的测定采用李益新化学发光法。脑组织水含量测定采用干湿重法结果过氧化脂质含量缺血组与假手术组，再灌注生理盐水对照组相比差异显著（Ｐ＜０．０１）。超氧化物歧化酶活性缺血组与假手术组，再灌注组与缺血组，氨氯地平组与生理盐水对照组相比均差异无显著性（Ｐ＞０．０５）。缺血组脑组织水含量无明显变化，而再灌注组明显增高，与缺血组相比差异显著（Ｐ＜０．０１），氨氯地平可明显降低脑缺血－再灌注脑组织水含量，与生理盐水对照组相比差异显著。病理组织学光镜观察，缺血组有明显的脑组织损伤，再灌注后损伤进一步加重，氨氯地平能使脑组织损伤明显减轻。结论脑缺血－再灌注期间脑内有自由基代谢紊乱，脑水肿形成。应用氨氯地平可使脑缺血－再灌注期间的脑组织自由基生?
OBJECTIVE: To observe the changes of brain biochemical metabolism, water content and histopathology in a replicated rat model of acute cerebral ischemia-reperfusion, and observe the effect of amlodipine, a new calcium channel blocker, on these indexes and On cerebral ischemia - reperfusion. Methods Male Wistar rats were treated with modified Pulsineli IV occlusion method. Both sides of bilateral common carotid artery were closed and the common carotid arteries were occluded except the sham-operation group. Determination of lipid peroxidation content using WSch Tsuchida method, determination of superoxide dismutase activity using Li Yixin chemiluminescence. Determination of water content in brain tissue using dry-wet weight results lipid peroxidation content of ischemic group and sham operation group, compared with reperfusion saline group, the difference was significant (P <0.01). There was no significant difference in SOD activity between ischemic group and sham operation group, reperfusion group and ischemic group, amlodipine group and saline control group (P> 0.05). There was no significant change in brain water content in ischemic group, while the reperfusion group was significantly higher than that in ischemic group (P <0.01). Amlodipine could significantly reduce the water content of cerebral ischemia-reperfusion brain tissue , Compared with the saline control group significant difference. Histopathological examination showed that there was obvious brain injury in the ischemic group and further aggravated after reperfusion. Amlodipine could significantly reduce brain injury. Conclusion There is disorder of free radical metabolism and brain edema in the brain during cerebral ischemia-reperfusion. Application of amlodipine can make cerebral ischemia-reperfusion brain tissue free radical generation?