摘要
目的:探讨NO是否参与脑缺血再灌期脑血管反应。方法:采用激光多普勒、电化学和超微病理方法分别测量和观察沙土鼠软脑膜微血管管径、NO含量和脑皮层微血管超微结构的变化。结果:脑缺血初期,细动脉呈线状收缩。缺血(50±10)min时,细动脉扩张至最大值,此时NO合成也增加至最大值。而后细动、静脉缓慢收缩,至缺血2h,细动、静脉呈节段性痉挛状态;同时,NO合成减少;微血管内皮细胞严重受损。缺血30min再灌流5min,NO分泌增加,细动、静脉扩张:缺血2h再灌流5min,NO合成减少,细动脉收缩。结论:轻度缺血时,NO合成增加,参与脑血管扩张反应;重度脑缺血时,沙土鼠微血管BC的结构严重受损,O2-NO通路中断,参与“盗血”反应。
Objective:To investigate if nitric oxide(NO)will be involved in the cerebral vascular response during cerebral ischemia -reperfusion. Methods; We measured the changes of pial - micrangium' s diameter, NO content and micrangium' s ultrastnicture of the cortex in gerbils by Laser Doppler and electrical chemistry. Results: A linear contraction of the arteriole was observed during initial ischemia. After ischemia for 50 + 10minutes, the arteriole dilated to the maximum value and NO content increased to the maximum, too. Then the micrangium contracted slowly. When ischemia for 2 hours, segmental spasticity of the micrangium was observed and NO content decreased. The endothelial cells of micrangium were severely injured. In the group that reperfusion was performed for Sminutes on the 30th minute of ischemia,NO content increased and the micrangium dilated.In the group that reperfusion was performed for 5 minutes on the 2nd hour of ischemia, NO content decreased and the arteriole contracted. Conclusion: NO content increased in mild cerebral ischemia, which indicated that NO takes part in the cerebral vascular response of dilatation. The endothelial cells of the micrangium in gerbils were severely injured in serious cerebral ischemia and the 02 - NO path was blocked, which indicated that NO takes part in the cerebral'stealing blood'response.
出处
《西南国防医药》
CAS
2003年第4期365-367,共3页
Medical Journal of National Defending Forces in Southwest China
