title: Cerebral vasospasm: a consideration of the various cellular mechanisms involved in the pathophysiology.
abstract: The cellular mechanisms responsible for cerebral vasospasm (CVS) occurring after subarachnoid hemorrhage (SAH) have been of major interest over the past 50 years. The present review describes how each of the discrete anatomic components that comprise the cerebral artery may contribute to the pathology of CVS. The blood extravasated after SAH is hemolyzed and undergoes degradation with resultant production of free radicals, known to be powerful initiators of vascular damage. An inflammatory response is generated activating both leukocytes and platelets with subsequent release of inflammatory agents. The cerebral artery affected by CVS undergoes phenotypic change involving both the endothelial and smooth muscle cells. In the endothelium the production of nitric oxide and prostacyclin is affected. In the smooth muscle cells signal transduction pathways that enhance the function of the contractile proteins and induce the upregulation of contractile receptors are activated. In parallel, there is evidence that nervous reflex pathways involving the trigeminal ganglion and the hypothalamus are activated. However, the relative contributions of each of the systems are speculative. Therapy may be directed at disrupting the cascade leading from the SAH insult to CVS or at overcoming the dysfunction incurred by CVS; possible therapeutical interventions are considered.
authors.affiliation: Department of Clinical Experimental Research, Glostrup University Hospital, Glostrup, Denmark. jacob.schwartz@dadlnet.dk
authors.forename: Jacob
authors.initials: J
authors.lastname: Hansen-Schwartz
mesh_terms: D001773:Blood Cells / Q000502:physiology*; D042783:Endothelial Cells / Q000502:physiology*; D006801:Humans; D032389:Myocytes, Smooth Muscle / Q000502:physiology*; D013345:Subarachnoid Hemorrhage / Q000150:complications / Q000473:pathology / Q000503:physiopathology; D020301:Vasospasm, Intracranial / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*