Mechanism of cardiac contracture during anoxic arrest using cardiopulmonary by-pass.

Cardiac contracture during anoxic cardiac arrest might result from a reduction in the adenosine triphosphate or from an accumulation of cytoplasmic calcium. The present study was undertaken to test the hypothesis that the accumulation of cytoplasmic calcium is a factor in the anoxic myocardial contracture in a setting similar to that used during cardiac surgery, using cardiopulmonary bypass. Anoxic cardiac arrest was produced for 30 and 60 minutes in 7 dogs each, by clamping the ascending aorta, using cardiopulmonary bypass. At the end of anoxic period, aorta was declamped for reperfusion of the heart for 30 minutes of termination of anoxic cardiac arrest. Total tissue and intracellular electrolytes were determined before and at various intervals (0, 5, 15, 30 minutes) after termination of anoxic cardiac arrest. Thirty minutes of anoxic cardiac arrest produced a significant decrease in the mean aortic and left ventricular systolic pressures, and left ventricular dp/dt/IIP; and a significant increase in the cardiac index. Total tissue and intracellular Na, Ca, and K did not change significantly at the end of 30 minutes of anoxia and during 30 minutes of reperfusion. Anoxic arrest for 60 minutes resulted in cardiac contracture in all dogs. The total and intracellular Ca decreased significantly at the end of 60 minutes of anoxia and during 30 minutes of reperfusion. Total tissue and intracellular Na, although, did not change during anoxic arrest, it increased significantly at 15 and 30 minutes of reperfusion. Cardiac potassium did not change significantly during the whole period of experiment. These studies suggest that total and intracellular calcium did not increase above the control values during anoxic myocardial contracture in a setting similar to that used during cardiac surgery, using cardiopulmonary bypass.