采用家兔急性不完全性全脑缺血模型(三血管结扎法),观察缺血及缺血再灌注后血液及脑组织内NOS活性的变化.结果发现,缺血后10 min,血液内NOS活性开始上升,1 h 达高峰,4 h 恢复至正常;脑组织在缺血后NOS活性立即开始增高,1 h 达高峰,4 h 后NOS活性显著下降.缺血再灌注组,在复灌30、60 min 时 NOS活性均明显高于单纯缺血组.缺血前静脉注射钙拮抗剂尼莫地平10 μg/kg+1μg/(kg*min)×10 min 可明显降低缺血及缺血再灌注时血液和脑组织中NOS的活性.提示:脑缺血后,血液及脑组织内NOS活性均发生明显的改变,在缺血早期,其活性显著增高.钙拮抗剂尼莫地平对缺血及缺血再灌所致的NOS活性增高有明显的抑制.%The incomplete cerebral ischemia-reperfusion model was made by occlusion of both common carotid arteries and the left vertebral artery to study the changes of the activity of nitric oxide synthase (NOS) in blood and brain tissue. The results showed that 10 min after ischemia, the NOS in blood began to increase, reached its peak at 1 h and returned to normal at 4 h. The NOS in brain tissue was increased immediately after ischemia, reached its peak at 1 h and obviously decreased at 4 h. In ischemia-reperfusion group, the NOS activity was higher 30 and 60 min after reperfusion than that in ischemia-alone group. Pretreatment with nimodipine [i.v, 10 μg/kg+1 μg/(kg*min) for 10 min], the activity of NOS was reduced significantly in blood and brain tissue. It was suggested that NOS activity in blood and brain tissue had a significant change following cerebral ischemia. At the early stage of ischemia, the NOS activity was significantly increased. Nimodipine could markedly inhibit the increase of NOS activity induced by ischemia and ischemia-reperfusion.
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