Role of Platelets in the Causation of Cerebral Vasospasm

J. M. RICE EDWARDS, BRIAN BULL, JOSEPH THOMPSON, and GEORGE AUSTIN (London) noted that the release of various vasoactive substances from platelets was thought to account for cerebral vasospasm after subarachnoid haemorrhage. That this was so in acute experimental vasospasm was confirmed by experiments on the cat's basilar artery in vivo. It had been shown that agents inhibiting the release phenomenon prevented spasm even when blood coagulated normally. It was, however, doubtful whether the release phenomenon was implicated in the delayed chronic vasospasms seen in humans after subarachnoid haemorrhage, but examination of the adventitia of cerebral vessels in monkeys with prolonged vasospasm did show that platelets adhered to the vessels and might well be able to influence the artery walls. It was suggested that delayed chronic vasospasm might be caused not by the release of vasoactive substances such as 5-hydroxytryptamine (because this was released rapidly and early) but by the release of substances during the disintegration of platelet lysosomes, which had an injurious effect on vessel walls.