The pharmacology of cerebral vasospasm.
About 3 days after subarachnoid hemorrhage the cerebral blood vessels often undergo a sustained constriction (cerebral vasospasm) which is associated with increased morbidity and mortality. Examination of the literature suggests that interactions of hemoglobin, various prostaglandins, and perhaps some other agents are responsible for this condition, which is apparently associated with endothelial damage or other structural changes. The most promising therapy involves treatment with calcium antagonists.
D002121:Calcium Channel Blockers / Q000494:pharmacology; D002395:Catecholamines / Q000502:physiology; D002561:Cerebrovascular Disorders / Q000503:physiopathology; D003327:Coronary Disease / Q000150:complications; D006801:Humans; D002532:Intracranial Aneurysm / Q000150:complications; D002546:Ischemic Attack, Transient / Q000188:drug therapy*; D009119:Muscle Contraction / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000503:physiopathology; D011453:Prostaglandins / Q000502:physiology; D012701:Serotonin / Q000502:physiology; D014665:Vasodilator Agents / Q000494:pharmacology
D002121:Calcium Channel Blockers; D002395:Catecholamines; D011453:Prostaglandins; D014665:Vasodilator Agents; D012701:Serotonin