Cerebral vasospasm - A consideration of the various cellular mechanisms involved in the pathophysiology
Cerebral vasospasm - A consideration of the various cellular mechanisms involved in the pathophysiology
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DOI：
10.1385/ncc:1:2:235
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发表时间：
2004-01-01
影响因子：
3.5
通讯作者：
Hansen-Schwartz, J
中科院分区：
文献类型：
--
作者：
Hansen-Schwartz, J
脑血管痉挛的细胞机制。(CVS)在过去的50年中，蛛网膜下腔出血（SAH）后发生的蛛网膜下腔出血（SAH）一直是主要关注的问题。本综述介绍了如何每个离散的解剖组成部分，包括脑动脉可能有助于CVS的病理。SAH后外渗的血液发生溶血并降解，从而产生自由基，已知自由基是血管损伤的强有力引发剂。产生炎症反应，激活白细胞和血小板，随后释放炎性物质。CVS影响的脑动脉经历了涉及内皮细胞和平滑肌细胞的表型变化。在内皮细胞中，一氧化氮和前列环素的产生受到影响。在平滑肌细胞中，增强收缩蛋白的功能并诱导收缩受体上调的信号转导途径被激活。同时，有证据表明，涉及三叉神经节和下丘脑的神经反射通路被激活。然而，每个系统的相对贡献是推测性的。治疗可能是针对破坏级联导致SAH侮辱CVS或克服CVS引起的功能障碍，可能的治疗干预措施被认为是。
The cellular mechanisms responsible for cerebral vasospasm. (CVS) occurring after subarachnoid hemorrhage (SAH) have been of major interest over the past 50 years. The present review describes how each of the discrete anatomic components that comprise the cerebral artery may contribute to the pathology of CVS. The blood extravasated after SAH is hemolyzed and undergoes degradation with resultant production of free radicals, known to be powerful initiators of vascular damage. An inflammatory response is generated activating both leukocytes and platelets with subsequent release of inflammatory agents. The cerebral artery affected by CVS undergoes phenotypic change involving both the endothelial and smooth muscle cells. In the endothelium the production of nitric oxide and prostacyclin is affected. In the smooth muscle cells signal transduction pathways that enhance the function of the contractile proteins and induce the upregulation of contractile receptors are activated. In parallel, there is evidence that nervous reflex pathways involving the trigeminal ganglion and the hypothalamus are activated. However, the relative contributions of each of the systems are speculative. Therapy may be directed at disrupting the cascade leading from the SAH insult to CVS or at overcoming the dysfunction incurred by CVS; possible therapeutical interventions are considered.