Cellular and molecular events of ischemic brain damage.
Many events occurring during and after cerebral ischemia are well known, but they are not known enough to fully elucidate the mechanisms of brain damage. Energy failure alone cannot explain the functional damage occurring during the reperfusion phase, and, at present, four features of the ischemic and postischemic brain are the focus of interest: development of acidosis, calcium overload, free radical formation, and nitric oxide overproduction. It is likely that these events, perhaps with other less known ones, contribute altogether to the occurrence of irreversible damage. An understanding of them might lead to the development of a drug, or a drug cocktail, able to counteract ischemic lesions.
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Institute of Pharmacology, University of Pavia, Italy.
Torri
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Marzatico
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D000138:Acidosis / Q000378:metabolism / Q000503:physiopathology*; D001921:Brain / Q000378:metabolism / Q000503:physiopathology; D001927:Brain Diseases / Q000378:metabolism / Q000503:physiopathology; D002545:Brain Ischemia / Q000378:metabolism / Q000503:physiopathology*; D002118:Calcium / Q000378:metabolism; D005260:Female; D005609:Free Radicals / Q000378:metabolism; D005947:Glucose / Q000378:metabolism; D006801:Humans; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism
D005609:Free Radicals; D009569:Nitric Oxide; D005947:Glucose; D002118:Calcium