脑缺血时微血管管径与一氧化氮释放的相关性(英文)

Correlation between the microvascular diameter and the release of nitric oxide in cerebral ischemia

背景:脑缺血时一氧化氮合成增加,参与脑缺血时脑血管扩张反应,但其释放规律及其与脑血管管径的相关性尚需深入研究。目的:探讨脑缺血时微血管管径与一氧化氮释放的关系。设计:随机自身对照研究。地点和对象:实验实施于解放军第三军医大学中心实验室。成年蒙古沙土鼠8只结扎双侧颈总动脉,制定全脑缺血模型。方法:采用激光多普勒和电化学方法,测量沙土鼠软脑膜微血管管径和一氧化氮的变化。主要观察指标:微血管管径和一氧化氮的变化。结果:脑缺血时,软脑膜细动脉立即收缩成线状,5min后开始舒张,缺血(40±10)min时,软脑膜细动脉扩张至最大值(56±16)μm,而后缓慢收缩;细动脉内的一氧化氮于缺血始合成增加,呈周期间断性释放,周期间隔为5～8min,持续时间3～5min,缺血10～40min,一氧化氮增至最大值(302±88)pA,而后逐渐减少,二者变化具有正相关性(r=0.886,P<0.001)。结论:脑缺血时一氧化氮分泌调控脑微血管舒缩功能。

BACKGROUND:The synthesis of nitric oxide(NO) increases under cerebral ischemia,which participates in cerebrovascular dilative reaction during cerebral ischemia.However,there is a need of thorough researches on the release disciplinary of NO and the correlation between NO and cerebrovascular diameter. OBJECTIVE:To investigate the correlation between the microvascular diameter and NO in cerebral ischemia. DESIGN:A randomly self controlled study. SETTING and SUBJECTS:Settings:Central laboratory of the Third Military Medical University of Chinese PLA.Subjects:Common carotid arteries on both sides were ligated in all 8 adult Mongolia gerbils to establish cerebral ischemia model. METHODS:The changes of pial microvascular diameter of gerbils were measured by Laser Doppler and the changes of NO were measured by electrochemistry. MAIN OUTCOME MEASURES:Changes of microvascualr diameter and NO. RESULTS:The pial microarteries contracted in line immediately after cerebral ischemia and began to relax in 5 minutes.And the maximum relaxation value of(56±16) μm was reached at(40±10) minutes after ischemia.Then they started to contract slowly.The synthesis of NO increased in the microartery of pia mater since cerebral ischemia,which released in cycles with 5 to 8 minutes of intervals and lasted for 3 to 5 minutes.The NO increased to its maximum value of (302±88) pA at 10 to 40 minutes after ischemia.Then it gradually reduced, which positively correlated with microvascular diameters(r=0.886,P< 0.001). CONCLUSION:The NO release regulates vasomotor function in cerebral microvessels during cerebral ischemia.