Ischemic brain injury and cell calcium: morphologic and therapeutic aspects.
Histopathological data obtained from different experimental models of hypoxia and ischemia were evaluated in order to extend current knowledge of mechanisms responsible for delayed neuronal cell death. Special attention is given to the distribution of calcium (Ca2+) in vulnerable areas during the postischemic period. Between an initial defensive Ca2+ sequestration, which is completely reversible, and final toxic Ca2+ overload, which is associated with irreversible neuronal necrosis, important Ca2+ shifts could be demonstrated cytochemically. Such shifts occur mainly at excitatory presynaptic sites and seem to precede structural ischemic cell change in postsynaptic areas. Recent results obtained with some Ca2+ entry blockers indicate that prophylactic treatment and postischemic intervention prevent cytosolic Ca2+ overload and reduce delayed brain injury.
D000818:Animals; D001921:Brain / Q000098:blood supply* / Q000187:drug effects; D001927:Brain Diseases / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology*; D002545:Brain Ischemia / Q000517:prevention & control; D002118:Calcium / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000627:therapeutic use; D006624:Hippocampus / Q000187:drug effects / Q000648:ultrastructure; D000860:Hypoxia / Q000378:metabolism / Q000473:pathology*; D007511:Ischemia / Q000378:metabolism / Q000473:pathology*; D051381:Rats
D002121:Calcium Channel Blockers; D002118:Calcium