Following periods of bilateral cerebral ischemia in urethane‐anesthetized Mongolian gerbils, the metabolism of isolated brain mitochondria was assessed in an in vitro oxygenated medium in the presence of the substrates glutamate‐malate. Mitochondria from both control and ischemic brains were well coupled. Urethane‐anesthetized controls showed an early mild depression and a subsequent enhancement of State 3 respiration (ADP present) relative to awake controls. Respiratory activity in State 3, calculated per mol of cytochrome oxidase, was first depressed below control values following 60 minutes of ischemia; and a further decline, to 46 to 58% of control values, followed 90 to 120 minutes of ischemia. Mitochondrial calcium ion accumulation was depressed by ischemia of 2 hours in moribund animals. In contrast, a significant degree of cerebral edema was observed with ischemia of only 30 minutes' duration. Respiration of brain mitochondria appears relatively resistant to irreversible impairment following cerebral ischemia.
ASJC Scopus subject areas
- Clinical Neurology