The pathophysiology of cerebral vasospasm, and pharmacological approaches to its management.
Numerous neurotransmitters, autocoids, and blood constituents or breakdown products have been shown to constrict the cerebral vasculature, and have therefore been implicated in the aetiology of cerebral vasospasm. Substances in combination may also act synergistically. Because of the multifactorial causes of vasospasm, the main causative agent may also be different in various subgroups of patients, leading to differential sensitivities to potential treatments. The contraction of vascular smooth muscle is ultimately caused by an increase in the intracellular concentration of free calcium ions. Mechanical, osmotic, or ischaemic trauma may also result in calcium overloading with development of contracture. Many "rational" pharmacological approaches to the treatment of vasospasm have been proposed, but clinical experience has so far been disappointing; agents active against only one possible causative factor may possess too specific a mechanism of action to control spasm caused by several agents simultaneously. A new group of drugs, the calcium antagonists, has selective and potent relaxant actions against the contractions of cerebral vessels produced by a wide range of agonists. They may be of therapeutic use in both the prophylaxis and treatment of cerebral vasospasm.
D002121:Calcium Channel Blockers / Q000627:therapeutic use; D006801:Humans; D002546:Ischemic Attack, Transient / Q000188:drug therapy / Q000503:physiopathology*
D002121:Calcium Channel Blockers