Mitochondrial respiration, succinate dehydrogenase coenzyme Q reductase, and myosin B were investigated in ischemic myocardium from experimental myocardial infarction in dogs. Respiratory control ratio of mitochondria was impaired by ischemia at 60 min after coronary ligation, and oxygen consumption was inhibited 120 min later. Enzyme activity of succinate dehydrogenase coenzyme Q reductase was decreased at 6 hr after coronary ligation. Calcium ion sensitivity of myosin B declined 12 hr after coronary ligation. However, adenosine triphosphatase activity of myosin A from infarcted myocardium was not different from that of the intact one. These results suggest that interaction in the sequence of enzyme complexes was first impaired in ischemic myocardium and that deterioration of enzyme activity was then manifested.

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PubMedDate not supplied

Features of lysosomal proteolytic enzyme activity in infarcted myocardium.

Myocardial infarction was produced in dogs to investigate the behavior of cardiac lysosomal enzymes; acid protease and beta-glucuronidase activities were measured in whole myocardial homogenate and 30,000 X g supernatant fractions. Total activity of acid protease in the whole homogenate of the myocardium increased after 1 hr of infarction and showed maximal value after 6 hr, while in the 30,000 X g supernatant fraction the activity began to increase after 3 hr and reached the maximal level by 24 hr. Total beta-glucuronidase activity in the whole homogenate decreased during the initial 3 hr after myocardial infarction and markedly increased after 12 hr. The activity in the 30,000 X g supernatant fraction showed corresponding changes. These findings that the increase in whole homogenate activity preceded that in the 30,000 X g supernatant fraction may support the hypothesis that lysosomal enzymes may be newly synthesized and then solubilized in the infarcted myocardium.

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PubMedDate not supplied

Experimental studies on cardiac arrhythmias with special reference to fibrillation in heart cell culture.

Fibrillation-like beating of cardiac muscle cells in culture was induced by altering the concentrations of various ions. Fine structural changes of cell membrane and intercellular alteration of cardiac muscle cells appeared to be more prominent in cells with fibrilliation-like beating than in others. From the results of the present study, it may be concluded that fibrillation-like beating may occur in the presence of altered concentrations of certain ions, accompanied by fine structural changes in the cells.

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