一氧化氮在脑血管痉挛的研究进展

Research Progress of Nitric Oxide in Cerebral Vasospasm

脑血管痉挛(CVS)是蛛网膜下腔出血(SAH)后主要的致残、致死原因,目前认为血凝块是出现CVS的始动因素,造成血管收缩因子增加和舒张因子减少,不能维持正常的血管张力。SAH后脑血管舒张因子一氧化氮(NO)减少可能是CVS发生的重要因素之一,NO可能参与缓解脑血管痉挛、促进神经保护、抗微血栓、促进内皮细胞功能等。前期实验研究表明,缝隙连接参与脑血管舒缩功能,SAH后血管缝隙连接蛋白表达发生改变,引起一系列的病理生理改变。因此,NO可能是SAH后CVS的治疗靶点。

Cerebral vasospasm (CV S) after subarachnoid hemorrhage (SA H ) is associated with severe mortality and morbidity. Many believe that the blood clots lead to the initiation of CVS, the potential imbalance between vasoconstricting and vasodilating influences on vascular tone. The reduction of nitric oxide (NO) is one of the most important inducements in the pathogenesis of CVS. NO has been implicated in eliminating vasospasm,facilitating neuroprotection,anti-microthrombosis and promoting endothelial cell function. Previous studies have shown that the gap junction is involved in the cerebrovascular vasomotion and the changes in gap junction protein expression led to a series of pathophysiological changes. Therefore,NO may be a therapeutic target for CVS after SAH.