Analysis of the microcirculatory disturbance in cerebral ischemia

本研究在脑缺血微循环障碍的病理生理学和治疗方面提供了以下三方面的重要信息：1)局灶性脑缺血时一氧化氮(NO)的产生。结果表明，脑缺血2小时和缺血2小时后再灌流30分钟，脑组织中NO_3~-含量显著升高。N-硝基-L-精氨酸(L-NAME，20 mg/kg)可阻断NO_3~-的这种增加。2)SOD改善微循环。给予重组人铜锌超氧化物歧化酶使大鼠大脑中动脉闭塞后3小时血浆灌流的微血管长度增加。3)白细胞作为缺血脑内自由基的来源。环磷酰胺诱导大鼠外周血白细胞减少(1180/mm^3)。大鼠大脑中动脉闭塞3h后，缺血侧脑片的化学发光强度明显低于正常白细胞计数(5180个/mm~3)。

This study presented the following three important informations on the pathophysiology and treatment of the microcirculatory disturbances in cerebral ischemia.1) Production of nitric oxide (NO) in focal cerebral ischemia.The levels of nitrate (NO_3) and nitrite (NO_2) in the jugular venous blood in rat focal cerebral ischemia were determined by Griess reaction. The results demonstrated the levels of NO_3^- were significantly increased at 2 hours of ischemia and at 30min reperfusion after 2 hours of ischemia. This increase in NO_3^- was blocked by N^G-nitro-L-arginine (L-NAME,20mg/kg).2)Improvement of microcirculation with SOD.The administration of recombinant human Cu, Zn-superoxide dismutase increased the length of plasma-perfused microvessels as was analyzed at 3 hours after occlusion of the middle cerebral artery in rats.3)Leukocytes as a source of free radicals in ischemic brain.Peripheral leukocytopenia (1,180/mm^3) was induced by cyclophosphamide in rats. The chemiluminescence of the slices of the ischemic hemispheres obtained at 3 hours of middle cerebral artery occlusion in those rats was significantly reduced as compared to that of normal leukocyte count (5,180/mm^3).