Influence of Experimental Subarachnoid Hemorrhage on Nicotine-induced Contraction of the Rat Basilar Artery in Relation to Arachidonic Acid Metabolites Signaling Pathway

Conclusions: One week after exposure to SAH, PLC, sPLA2, and COX-2 activity were enhanced and cPLA2 activity was inhibited. One hour after exposure to SAH, PLC activity was enhanced and cPLA2 and iPLA2 activity was inhibited. Such changes of inflammatory arachidonic acid metabolites by smoking after SAH may play important roles in fatal cerebral circulatory disorders, suggesting important implications for the etiology and pathogenesis of SAH.
Source: Journal of Stroke and Cerebrovascular Diseases - Category: Neurology Authors: Tags: Original Articles Source Type: research