The relevance of in vitro smooth muscle experiments to cerebral vasospasm.
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.
D000199:Actins / Q000502:physiology; D000205:Actomyosin / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000378:metabolism; D002118:Calcium / Q000378:metabolism; D002147:Calmodulin / Q000378:metabolism; D002560:Cerebrovascular Circulation; D006801:Humans; D002546:Ischemic Attack, Transient / Q000503:physiopathology*; D008564:Membrane Potentials; D009119:Muscle Contraction; D009131:Muscle, Smooth, Vascular / Q000503:physiopathology*; D009218:Myosins / Q000502:physiology
D000199:Actins; D002147:Calmodulin; D000255:Adenosine Triphosphate; D000205:Actomyosin; D009218:Myosins; D002118:Calcium