| pubmed-article:9157370 | pubmed:abstractText | The purpose of the study was to examine the pattern of changes revealed in the metabolic reactions in the cerebral mitochondria, oxidizing succinates in acute circulatory hypoxia under the influence of hyper- and normoxic conditions of an experiment. Following 3.5 hours of acute circulatory hypoxia in the cerebral mitochondria which were resistant to bilateral carotid occlusion, rats showed increased succinate-dependent energy production, followed by compensatory inhibition of succinate dehydrogenase. The normoxic conditions of the cerebral mitochondrial investigations preserved succinate-dependent and transaminase respiratory fractions of organelles which were inhibited under hyperoxic conditions of an experiment. This improves more objective assessment of the responses of the mitochondrial oxidation system on the pathology model under study. | lld:pubmed |
