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目的 探讨氨基胍 (AG)对脑缺血 再灌注 (IR)神经细胞损伤的影响。方法 用线栓法制作大鼠局灶性脑缺血 再灌注模型 ,动物缺血 2小时后给予腹腔注射AG 10 0mg·kg-1,取不同再灌注时间测定大鼠脑匀浆NOS活性、髓过氧化物酶 (MPO)活性和脑梗死体积。结果 再灌注后 12～ 72小时 ,AG显著降低了iNOS活性 ,且于再灌注后 2 4小时达最大抑制率。再灌注后 2 4～ 72小时 ,AG减少髓过氧化物酶 (MPO)含量。再灌注后 2 4～ 72小时 ,AG减少梗死体积。结论 AG对脑缺血 再灌注神经细胞损伤具有一定的保护作用。
Objective To investigate the effect of aminoguanidine (AG) on neuronal injury after cerebral ischemia-reperfusion (IR). Methods The model of focal cerebral ischemia-reperfusion in rats was established by thread occlusion method. The animals were given intraperitoneal injection of AG 10 0 mg · kg-1 2 hours after ischemia and the reperfusion time was used to measure the activity of NOS, Peroxidase (MPO) activity and infarct volume. Results After 12-72 hours after reperfusion, AG significantly reduced iNOS activity and reached the maximum inhibition rate at 24 hours after reperfusion. After 24 to 72 hours after reperfusion, AG decreased the content of myeloperoxidase (MPO). 24 to 72 hours after reperfusion, AG reduced infarct volume. Conclusion AG has a protective effect on nerve cell injury after cerebral ischemia-reperfusion.