During anoxia, degenerative changes occur so rapidly in the mammalian brain that within a few minutes ion homeostasis is lost, energy sources are depleted and recovery becomes questionable. This vulnerability is characteristic of vertebrate brains in general and is likely a consequence of the high energy demand of brain tissues. Studies of these degenerative processes and of brain anaerobic metabolism are hindered by the rapidity of anoxia-induced changes. In order to investigate anaerobic metabolism, and to define the compensatory processes that promote survival during anoxia, an animal model is needed that has a high brain anaerobic capacity. The turtle is ideal in this regard. In studies reported here, mitochondrial reduction/oxidation reactions in turtle brain were monitored by reflection spectrophotometry, tissue oxygen tension by polarography, ion homeostasis by potassium-selective microelectrodes and metabolite concentrations by assay of freeze-trapped brain samples. Differences between rat and turtle brain were found in the relationship between cytochrome oxidase and tissue oxygenation. In addition, in the turtle brain lactate production was initiated before cytochrome oxidase became fully reduced. These findings suggest a relationship between mitochondrial redox status and anaerobiosis. Maintenance of ion homeostasis and ATP levels suggest that the turtle brain compensates for prolonged anoxia by increased glycolysis, depletion of CP stores and decreased ATP consumption. The identification of anoxia-induced compensatory activity in turtle brain models should offer new insights into anaerobic processes and mechanisms for anoxic brain survival in the mammal.
|Original language||English (US)|
|Number of pages||15|
|State||Published - Jan 1 1985|
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)