Mitochondrial Respiration of Experimentally Produced Ischemic Heart Muscle in Dogs

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Abstract
The mitochondrial respiration in experimentally produced myocardial infarction or ischemic heart was investigated. In myocardial infarction, disturbances of respiration appeared 15 min. after the coronary artery occlusion, which was recognized as the deterioration of respiratory control ratio as result of the acceleration of O2 consumption rate in state 4. Deterioration of respiratory control ratio was also recognized in mitochondria of the heart which was stimulated electrically, but was not recognized in the heart mitochondria which were prepared from the heart stored in anoxic state without beating. Mg-induced ATPase activity of the infarcted heart mitochondria was higher than that of the intact heart mitochondria. It was assumed from these results that disturbance of the respiration of infarcted heart mitochondria was attributed to the uncoupling of oxidative phosphorylation.

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