Influence of Blood Volume on Cerebrospinal Fluid Levels of Arachidonic Acid Metabolites after Subarachnoid Hemorrhage: Experimental Study on the Pathogenesis of Cerebral Vasospasm

Publisher Website
Google Scholar
Abstract
Based on accumulating data indicating the important role of arachidonic acid metabolites in the pathogenesis of cerebral vasospasm, we examined the influence of alterations in blood volume on the cerebrospinal fluid (CSF) level of the subarachnoid hemorrhage (SAH). Three separate injections of autologous blood into the cisterna magna of dogs within subarachnoid hemorrhage (SAH). Three separate injections of autologous blood into the cisterna magna of dogs within 72 hours were performed. Three experimental groups were formed, with an overall injected blood volume of 6, 9, and 12 ml. Arterial spasm was verified by comparison of the angiographic diameter of the basilar artery on Day 8 vs. Day 1. Additionally, light microscopic, scanning and transmission electron microscopic, and freeze cracking technique examinations of the basilar artery demonstrated the typical morphological features of proliferative vasculopathy. Increasing the volume of experimental SAH led to a linear decrease of the mean vessel diameter from 45% to 53% and finally to 75% of normal. Parallel to the reduction of angiographic vessel lumen, a volume-dependent significant increase of all three eicosanoids was demonstrated. A deficiency of prostacyclin concentration during the course of the experiment was not observed. Despite highly elevated CSF levels of vasodilating prostacyclin, however, severe angiographic constriction of the basilar artery occurred in the presence of high concentrations of TXA2 and PGE2. It is concluded that increasing volumes of SAH led to a concomitant release of arachidonic acid metabolites during posthemorrhagic clot lysis. From our data, it seems questionable whether a prostacyclin deficiency is an important underlying factor for the development of cerebral spasm. Instead, elevation of spasmogenic eicosanoids, especially TXA2 and PGE2, is more likely to play a major role in the multifactorial pathogenesis that finally leads to delayed cerebral vasospasm.