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研究局灶性脑缺血和再灌注期一氧化氮合酶的活性和局部脑血流量的动态变化.用改良Koizumi’s大鼠局灶性脑缺血和再灌注模型及改良Bredt和Snyder’s法测定了缺血和再灌注期缺血侧脑组织一氧化氮合成酶(NOS)总活性,并同步以激光多普勒血流仪(LDF)对缺血周边区局部脑血流量(ICBF)进行了测定.结果:缺血早期,缺血侧半球脑组织NOS活性急剧升高至缺血前2～3倍(P<0.01),缺血后期NOS活性降至缺血前水平(P>0.05);缺血10～20 min缺血周边区ICBF回升至缺血前的30%左右(P<0.05);再灌注10min出现高灌,30min后持续下降.提示:缺血期因为钙内流,使NOS活性剧增,有利于维持缺血区和周边区的脑血流量,但过量产生的NO可造成细胞损伤.再灌注期由于表达增加,加之钙超载使NOS活性再度升高,NO可与再灌注期大量产生的超氧阴离子反应生成毒性自由基而损伤细胞.
To study the dynamic changes of nitric oxide synthase activity and regional cerebral blood flow in focal cerebral ischemia and reperfusion period.Methods: The model of focal cerebral ischemia and reperfusion in Koizumi’s rats was established and the modified Bredt and Snyder’s The total activity of nitric oxide synthase (NOS) in the ischemic brain tissue during ischemia and reperfusion was measured. The regional cerebral blood flow (ICBF) in peripheral ischemic area was measured by laser Doppler flowmetry (LDF) Results: In the early stage of ischemia, the activity of NOS in the ischemic hemisphere increased sharply to 2 ~ 3 times before ischemia (P <0.01), and the activity of NOS in the ischemic hemisphere decreased to the level before ischemia (P> 0.05). The ICBF of ischemic peripheral zone in 10-20 min of blood returned to about 30% before ischemia (P <0.05), high perfusion occured 10 min after reperfusion and continued to decline after 30 min, suggesting that NOS activity However, overproduction of NO can cause cell injury.As the increased expression of reperfusion and the increase of calcium overload lead to the increase of NOS activity, NO can be associated with reperfusion A large number of superoxide anion generated reaction of toxic free radicals damage cells.