An in vitro study of prolonged vasospasm of a rabbit cerebral artery.

Longitudinal stretch of the rabbit basilar artery produces local injury followed by prolonged circular constriction. After stretching and rapid release in vitro localized constrictions promptly occurred. This could be prevented by prior treatment with cyanide or calcium-free solution. Once produced, constrictions persisted for more than 72 hours. Previously induced constriction was not reversed by treatment for two hours with cyanide or by removing calcium. Histological observation indicated that constricted areas were associated with a discrete circumferential rupture of the internal elastic lamina and disruption and thinning of the underlying media. Specific catecholamine fluorescence at the adventitio-medial junction was unchanged in constricted areas. The relationship between smooth muscle cell length and resting tension of artery segments with and without constrictions was compared. Segments with constrictions had a shorter muscle length for any given resting tension, which confirms that constriction was not due to passive collapse of the vessel wall. These findings suggest that injury of cerebrovascular smooth muscle may result in essentially irreversible vasoconstriction. Such a mechanism could contribute to the pathogenesis of prolonged cerebral vasospasm after SAH or traumatic injury to the cerebrum.