Brain ischaemia, calcium and calcium antagonists.
There is a great similarity between the loss of respiratory activity of isolated cerebral mitochondria which have been submitted to ischaemia in vivo and the loss of activity following the incubation of normal cerebral mitochondria in the presence of Ca2+. These observations may imply that Ca2+ could play an important role in the pathogenesis of the cellular changes which accompany ischaemia. Studies in vitro with Ca2+ antagonists (diltiazem, nifedipine, perhexiline and verapamil) have shown these agents to possess a powerful vasodilatatory action but to be incapable of reversing the loss of functional activity of isolated mitochondria from the ischaemic brain. Although the treatment of a primary focal cerebral ischaemia by Ca2+ antagonists does not seem promising, these agents may be of considerable interest in the therapy of cerebral ischaemia secondary to vasospasm.
D000818:Animals; D001921:Brain / Q000648:ultrastructure; D002545:Brain Ischemia / Q000188:drug therapy* / Q000503:physiopathology; D002118:Calcium / Q000494:pharmacology / Q000502:physiology*; D002121:Calcium Channel Blockers / Q000627:therapeutic use*; D002546:Ischemic Attack, Transient / Q000188:drug therapy; D008297:Male; D008928:Mitochondria / Q000187:drug effects; D051381:Rats
D002121:Calcium Channel Blockers; D002118:Calcium