Why the study?
Does coronary circulation support prevent carbohydrate metabolism changes in heart muscle during artificially induced arrhythmias?
Does coronary circulation support prevent carbohydrate metabolism changes in heart muscle during artificially induced arrhythmias?
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Metabolic changes in the heart during ventricular and atrial arrhythmias are primarily driven by anoxia rather than the arrhythmias themselves.
Changes in the ratio phosphorylase a/total phosphorylase in heart muscle, as well as the myocardial concentrations of glycogen, glucose-6-phosphate (G-6-P), lactate, pyruvate, fructose-l,6-diphosphate (FDP), dihydroxyacetone phosphate (DHAP), were followed during artificially induced ventricular tachycardia, and ventricular fibrillation, and atrial fibrillation.These experiments were carried out with and without support of the coronary circulation. When coronary circulation was not maintained, active phosphorylase increased, then diminished in heart muscle during ventricular and atrial fibrillation and during ventricular tachycardia. The myocardial concentration of lactate and glucose-6-phosphate rose, while that of glycogen dim inished. No appreciable changes occurred in the concentration of fructose-1,6-diphosphate, dihydroxyacetone phosphate, and pyruvate. These changes were similar to those reported on skeletal muscle. When coronary circulation was maintained, no changes in carbohydrate intermediates or in phosphorylase a activity were recorded. These results demonstrate that the metabolic changes encountered in heart muscle during these arrhythrnias are the result of anoxia.
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Klarwein et al. (1961) studied this question.
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