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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 m in,血液内 NOS活性开始上升 ,1h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 ,1h达高峰 ,4 h后 NOS活性显著下降。缺血再灌注组 ,在复灌 3 0、 60 m in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。
Rabbit acute incomplete global cerebral ischemia model (three-vessel ligation) was used to observe the changes of NOS activity in blood and brain tissue after ischemia and reperfusion. The results showed that NOS activity in blood started to rise 10 min after ischemia, peaked at 1 h and returned to normal at 4 h. NOS activity in brain tissue immediately increased after ischemia, peaked at 1 h and decreased significantly after 4 h . In ischemia-reperfusion group, NOS activity was significantly higher than that in ischemia-reperfusion group only at 30 and 60 mins reperfusion. Pretreatment with nimodipine (10 μg / kg + 1 μg / (kg · min) × 10 min), a calcium antagonist, can significantly decrease the activity of NOS in blood and brain tissue during ischemia and reperfusion. Tip: After cerebral ischemia, blood and brain tissue NOS activity were significantly changed, early in the ischemia, the activity was significantly higher. Nimodipine, a calcium antagonist, significantly inhibited the increase of NOS activity induced by ischemia and reperfusion.