缺血性中风是一种严重威胁人类健康的疾病，恢复脑部的血液供应是治疗中风的前提。然而，在血管再通后的中风病人中仍广泛出现大脑血液无复流或低灌注的现象，这严重干扰了病人的预后。目前血管平滑肌(VSMC)在中风前后对血流调控的动态变化及细胞作用机制仍不明了。我们前期的研究结果发现血管阻塞将导致大脑中动脉上的VSMC发生异常紧缩，而其内部存在的大量线粒体很有可能对VSMC的收缩力具有重要的调节作用。由此我们提出科学假设：线粒体是中风发生时VSMC缺血缺氧损伤的感受器，继而引发VSMC舒缩力改变和大脑血流微循环的异常。本研究结合活细胞成像及双光子活体动物成像，从时间空间变化的角度在体外、离体、体内三个水平研究VSMC线粒体对中风发生时脑部血流调控的细胞及分子机制，探索通过调节VSMC线粒体活性改善中风后脑部血液供给的方法。本研究将为缺血性中风后恢复脑部供血提供新的理论依据及治疗策略。

Ischemic stroke is a serious threat to human health, restoring cerebral blood supply is the first priority of ischemic stroke treatment. However, the phenomenon of no-reflow or hypoperfusion could still be found in the brain after recanalization extensively, which disturb the recovery of patients severely. At present, the dynamic changes and cellular mechanism of vascular smooth muscle cell (VSMC) on cerebral blood flow regulation during ischemic stroke still remains elusive. Our previous work had found that vascular occlusion will lead to the abnormal stiffness of VSMC on the middle cerebral artery, and the large number of mitochondria in the VSMC may play an important role in regulating the contractility of VSMC. Therefore, we propose a scientific hypothesis: mitochondria are the censors of VSMC during ischemic stroke, which in turn lead to the changes of VSMC’s contractility and further destroy of cerebral blood supply. In this study, using the technique of living cell imaging and two-photon live animal imaging, we’ll study the cellular and molecular mechanism of VSMC mitochondria on the regulation of cerebral blood flow during ischemic stroke in three levels, in vitro, ex vivo and in vivo temporally and spatially. In addition, we’ll find a way to improve cerebral blood flow through VSMC mitochondria manipulation. This project will provide a new theoretical basis and treatment strategy for restoring blood supply after ischemic stroke.