Stroke, Vol 16, 573-581, Copyright © 1985 by American Heart Association
GR Wellum, JW Peterson and NT Zervas
An overview of the possible factors that might contribute to the
development of cerebral vasospasm is presented, with particular emphasis on
the possibility that spasm arises from a malfunction of the regulatory or
contractile processes in smooth muscle cells. This possibility is
emphasized because the evidence for cellular damage and the delayed
occurrence of vasospasm are suggestive of pathological alteration. Data
regarding the development of spasm in vivo has been reviewed and, to the
extent possible, correlated with in vitro studies of cerebrovascular smooth
muscle contractility. Short-term in vitro studies of normal cerebral
arteries may be of little relevance to the prolonged and severe cerebral
vasoconstriction that occurs only after a delay of several days from the
initial insult.
ARTICLES
The relevance of in vitro smooth muscle experiments to cerebral vasospasm
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