A theory of the mechanism of cerebral vasospasm and its reversal, the role of calcium and cyclic AMP.
It is proposed that the basic mechanism of vasospasm which sometimes follows subarachnoid hemorrhage is dependent on increased free intracellular calcium ion produced by spasmogens from closely applied extravasated blood. Relaxation of this spasm occurs when the intracellular cyclic AMP levels are raised, resulting in sequestration of calcium ion by the vascular smooth muscle cell sarcoplasmic reticulum.
D001792:Blood Platelets / Q000378:metabolism; D001808:Blood Vessels / Q000187:drug effects; D001921:Brain / Q000098:blood supply; D003994:Bucladesine / Q000627:therapeutic use; D002118:Calcium / Q000378:metabolism*; D000242:Cyclic AMP / Q000378:metabolism*; D002546:Ischemic Attack, Transient / Q000188:drug therapy / Q000209:etiology / Q000378:metabolism*; D008959:Models, Neurological; D009119:Muscle Contraction / Q000187:drug effects; D009130:Muscle, Smooth / Q000378:metabolism; D011460:Prostaglandins F / Q000378:metabolism; D012701:Serotonin / Q000378:metabolism; D013345:Subarachnoid Hemorrhage / Q000150:complications; D013806:Theophylline / Q000627:therapeutic use
D011460:Prostaglandins F; D012701:Serotonin; D003994:Bucladesine; D013806:Theophylline; D000242:Cyclic AMP; D002118:Calcium