论文部分内容阅读
目的 研究尼莫地平对脑缺血再灌注后大鼠血脑屏障 (BBB)通透性的影响。方法 采用线栓法制作大鼠大脑中动脉闭塞的局灶性脑缺血模型。缺血 1h后再灌注 ,分别于缺血前及再灌注后静脉注射尼莫地平。采用免疫组织化学 SABC法 ,观察再灌注 12 h时 ,内源性免疫球蛋白 G(Ig G)在脑组织中的表达 ,比较缺血前注射尼莫地平组、未注射尼莫地平组及再灌注后注射尼莫地平组三组大鼠脑组织中 Ig G的表达水平。结果 未注射尼莫地平组大鼠 ,在再灌注 12 h时 ,缺血侧大脑半球纹状体及新皮层可见广泛的 Ig G表达。再灌注后注射尼莫地平组大鼠 ,Ig G的表达更加明显。缺血前注射尼莫地平组大鼠 ,Ig G的表达在新皮层仅见于微血管壁内 ,在纹状体可见局灶性 Ig G的表达。结论 脑缺血再灌注后注射尼莫地平可加重 BBB的损伤 ,使其通透性增加。缺血前注射尼莫地平 ,可使再灌注后 BBB的损伤减轻。
Objective To investigate the effect of nimodipine on the permeability of blood-brain barrier (BBB) in rats after cerebral ischemia-reperfusion. Methods The model of focal cerebral ischemia in middle cerebral artery occlusion rats was made by thread plug method. After 1h ischemia reperfusion, respectively, before ischemia and reperfusion after intravenous injection of nimodipine. Immunohistochemical SABC method was used to observe the expression of IgG in brain tissue at 12 h after reperfusion. Compared with nimodipine group before injection and nimodipine group before reperfusion The level of Ig G expression in brain tissue of three groups of rats injected with nimodipine after perfusion. Results In nimodipine-treated rats, extensive Ig G expression was found in striatum and neocortex of the ischemic hemisphere at 12 h after reperfusion. After reperfusion, the nimodipine group rats, Ig G expression more pronounced. In pre-ischemic Nimodipine group, the expression of Ig G was seen only in the microvessel wall in the neocortex, and focal Ig G expression was seen in the striatum. Conclusion The injection of nimodipine after cerebral ischemia and reperfusion can aggravate the injury of BBB and increase its permeability. Premedication of nimodipine can reduce the damage of BBB after reperfusion.