作者: V. Seifert , V. Kaever , D. Stolke , K. Resch , H. Dietz
DOI: 10.1007/978-3-642-71108-4_40
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摘要: The development of cerebral angiospasm following rupture an intracranial aneurysm is considered to be one the major causes morbidity and mortality in patients with subarachnoid hemorrhage (SAH) (20, 22, 29). Despite many clinical experimental studies there still no generally accepted treatment or prophylaxis vasospasm. complicated pathophysiological events which occur during pre–and postoperative course SAH may lead fatal arterial narrowing are only partially understood. Recent investigations have elucidated important role metabolites arachidonic acid, especially prostacyclin (PGI2) thromboxane A2 (TXA2), genesis vasospasm after (1–6, 13, 18, 26) (Fig. 1). delicate balance between PGI2, a. potent vasodilator inhibitor platelet aggregation, TXA2, a substance strong vasocon–stricting aggregating properties, thought essential for preservation tonus vasculature under physiological circumstances. During several pathological decreased synthesis PGI2. Thus relationship PGI2 TXA2 changed disproportionate concentration consequent aggregation