[Cerebral posthemorrhagic vasospasm. A sequential in vivo and in vitro study of the basilar artery of the rabbit]

Abstract

Subarachnoid hemorrhage (SAH) by multiple injections of autologous blood into the prepontine cistern of the rabbit induced angiographic visible vasospasm of the basilar artery. Vasoconstriction on day nine after SAH was 70.7%. The mean peak constriction was recorded on day one after SAH (53.7%). Papaverine (PPV) reversed acute vasospasm from day one to day three after SAH. Gradually increasing refractoriness of vasospasm to PPV on angiograms was seen between day four and day nine after SAH. PPV-refractoriness (in vivo) was positively correlated with increasing vessel wall stiffness (in vitro). In vitro investigations displayed a gradual and marked reduction in the maximum capacity of the vessel wall to develop active tone. Spontaneous increases in tone independent from exogenous chemical stimuli were recorded during the first two days after SAH. Tonic contraction to the maximum dose of serotonin was increased on day one, two and five respectively, and decreased from day six to day nine after SAH. Constrictor nerve influences on vascular tone as well as acetylcholine-induced vasorelaxation were consistently reduced over a nine day period after SAH. It is suggested that the initial cause of the arterial narrowing after SAH is the action of vasoactive substances released in the close vicinity of the arterial wall, which lead to tissue damage, abnormal tone, and an inflammatory response with fibrosis. Passive factors seem to dominate in chronic vasospasm.