Wiernsperger N
International Pharmacological Department, International Division, Lipha, Lyon, France.
J Cardiovasc Pharmacol. 1990;16 Suppl 3:S20-4.
Most evidence in the literature concerning the role of serotonin in ischemia originates from brain research. This is partly because the central nervous system is particularly prone to accumulation of 5-HT, due to the neuronal sources of the amine in addition to circulating 5-HT from platelets. In ischemia, platelet invasion, rupture of the blood-brain barrier, liberation of 5-HT from nerve terminals inside the vessel wall, and necrosis of serotonergic neurons favor local increases of the transmitter in the brain. The pathophysiological consequences include amplifications of processes such as vasoconstriction of major and collateral arteries, edema formation, platelet aggregation, and blood sludging. 5-HT2 receptors appear to be the major effector of these actions of serotonin, judging from experimental and clinical pharmacology data with specific or partial 5-HT2 serotonergic antagonists. This review summarizes current knowledge on the key role serotonin plays in the induction or consequences of brain ischemia.
文献中关于血清素在缺血中作用的大多数证据都来自脑研究。部分原因是，除了血小板循环中的5-羟色胺外，由于胺的神经元来源，中枢神经系统特别容易积累5-羟色胺。在缺血时，血小板入侵、血脑屏障破裂、血管壁内神经末梢释放5-羟色胺以及血清素能神经元坏死，都有利于脑内该递质的局部增加。病理生理后果包括诸如主要动脉和侧支动脉血管收缩、水肿形成、血小板聚集和血液淤滞等过程的放大。从使用特异性或部分5-羟色胺能拮抗剂的实验和临床药理学数据判断，5-羟色胺2受体似乎是血清素这些作用的主要效应器。本综述总结了关于血清素在脑缺血的诱导或后果中所起关键作用的当前知识。
