Development of a novel therapeutic modality targeting G protein-coupled receptors for cerebral vasospasm after subarachnoid hemorrhage

蛛网膜下腔出血(SAH)后的脑血管痉挛是以脑动脉收缩延迟和延长为特征的，可引起脑缺血，从而决定SAH患者的生活和神经功能的预后。然而，脑血管痉挛的分子机制尚不清楚。在这项研究中，我们研究了SAH在激动剂诱导的兔痉挛脑动脉收缩中的特异性变化，并阐明了SAH后G蛋白偶联受体介导的血管收缩能力增强的一些调节机制。

Cerebral vasospasm after subarachnoid hemorrhage (SAH) is characterized by delayed and prolonged contraction of cerebral arteries, which may cause cerebral ischemia, thereby determining the prognosis of both life and neurologic function of SAH patients. However, the molecular mechanisms of cerebral vasospasm remain to be elucidated. In this study, we investigated SAH-specific changes in the agonist-induced contraction in the rabbit spastic cerebral arteries and elucidated some regulating mechanisms underlying the increased vascular contractility in G protein-coupled receptor-mediated contraction after SAH.