Cerebral Microthrombosis, Synthesis Imbalance of TXA2-PGI2, and Subarachnoid Focal Acidosis in the Pathogenesis of Symptomatic Cerebral Vasospasm
Numerous investigations of cerebral vasospasm (hearafter referred to as vasospasm) confirm the pathogenesis to be various and complicated. In accounting for the pathogenesis of vasospasm, it is our contention that subarachnoid focal acidosis resulting from anaerobic changes in subarachnoid clots may play a role in inducing multiple cerebral microthrombosis, which in turn induces cerebral ischemia or infarction by platelet aggregation caused by an imbalance in the synthesis of TXA2 and PGI2 (Fig. 1) [6–9]. In this paper, we tried to corroborate that contention in clinical studies focussed firstly on the pH of intracranial irrigation fluid for aneurysmal surgery during the vasospasm predilection period and, secondly, on the effectiveness of TXA2 synthetase inhibitors in the prevention of symptomatic vasospasm, and in histopathological studies of the brains of patients who died of subarachnoid hemorrhage.
KeywordsCerebral Aneurysm Cerebral Vasospasm Synthetase Inhibitor Symptomatic Vasospasm Angiographical Vasospasm
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