Oxygen consumption of the nonworking and potassium chloride-arrested dog heart.

Abstract

In 21 dogs on cardiopulmonary bypass with ventricles kept empty, the mean beating but nonworking myocardial O2 consumption (mVO2) was 3.8 ml/min per 100 g at a heart rate of 158 beats/min. After subsequent KCl arrest, the basal mVO2 was 1.74 ml/min per 100 g. To compare these values with the working situation, mVO2 was measured in the hearts before instituting bypass when the heart rate averaged 179 beats/min and arterial pressure averaged 108 mm Hg; mVO2 was 9.2 ml/min per 100 g. Atrioventricular dissociation was induced in 5 beating, nonworking hearts; electrical pacing at increasing heart rates produced a linear increase in mVO2. Extrapolation to zero heart rate yielded a value of 1.24 ml/min per 100 g which was not significantly different from the KCl arrest value of 1.25 ml/min per 100 g in the same hearts. These measurements permitted calculation of an energy expenditure per beat of 10.4 mJ/g. Subtraction of the basal value of 2.0 mJ/g yielded a value for energy of contraction of 8.4 mJ/g. The stress-independent component was an estimated 2.7 mJ/g. The basal mVO2 at normal perfusion pressure remained constant for arrest periods of at least 1 h. Perfusion with modified Krebs-Henseleit buffer caused a 30% reduction in the basal mVO2 despite maintained perfusion pressure, O2 supply in excess of consumption, coronary venous PO2 [partial pressure of O2] values > 60 mm Hg and the addition of amino acids. This finding may indicate deficient oxygenation of myocardial cells in hearts perfused with solutions lacking red cells.