脑血管痉挛（CVS）是动脉瘤性蛛网膜下腔出血（SAH）的严重并发症，致死致残率高，目前在临床上缺乏有效的治疗手段。既往研究发现钙离子内流导致的血管平滑肌收缩是SAH后CVS的重要原因。瞬时受体电位通道C（TRPC）是一种位于细胞膜上的离子通道蛋白，其中TRPC1和TRPC4是调控钙离子内流的主要亚型，因此本研究以这两种蛋白质功能作为切入点，从细胞、组织和活体三个层面构建SAH模型，应用RNAi、基因转染、给予药物，以及基因敲除等干预手段，结合膜片钳、血管张力评估、分子生物学技术与形态学观察，测定SAH环境下TRPC1和TRPC4的表达，观察血管平滑肌细胞、内皮细胞以及血管变化，检测钙离子电位水平和浓度，从而阐明TRPC1和TRPC4在CVS发生过程中的作用，预期研究结果将揭示血管平滑肌和内皮细胞钙离子稳态失衡的新机制和CVS相关异常信号通路的新途径，为SAH后CVS的临床治疗提供新的策略。

Cerebral vasospasm (CVS) is a serious complication of aneurysmal subarachnoid hemorrhage (SAH) with high mortality and morbidity. Since the pathogenesis remains elusive, no effective clinical therapeutic strategy for CVS is available now. Previous studies revealed that the contraction of vascular smooth muscle induced by calcium influx is a crucial cause for CVS after SAH. Also, transient receptor potential channel C (TRPC) is an ion channel protein located on the cell membrane, and it includes two subtypes TRPC1 and TRPC4 which can regulate the calcium influx. In this study, we take the special function of these two proteins as breakthrough point, and establish SAH model in cell, tissue and living animal model. The interventions of RNAi, gene transfection, medication and gene knockout are used in this study. Meanwhile, patch clamp, vascular tension evaluation, molecular biology and morphological observation techniques are applied to detect the TRPC1 and TRPC4's expressions, to observe the smooth muscle cells and vascular changes, and to quantify the calcium potential in SAH model. Finally, we can elaborate the roles of TRPC1 and TRPC4 in CVS. The expected study results will disclosure a new mechanism of calcium dyshomeostasis in vascular smooth muscle and an original abnormal signaling pathway in CVS. This study can provide us a novel clinical therapeutic strategy for CVS after SAH.