Changes in total and transmural coronary blood flow induced by ethanol

We studied the effects of ethanol on total coronary resistance and on the resistance across the left ventricular wall in the isolated empty beating heart of the dog. The coronaries were perfused with homologous fresh blood, thermoregulated at 37 degrees C and equilibrated with a gas mixture of O2 (95%) and CO2 (5%). Coronary flow distribution was measured with radioactive microspheres. In 22 experiments in which coronary flow was kept constant, ethanol (calculated concentration in the perfusing blood, 2.9 +/- 0.2 g . litre-1) produced a significant decrease in perfusion pressure (from 14.2 +/- 0.5 to 11.9 +/- 0.5 kPa, P less than 0.005). This decrease in perfusion pressure was not caused by metabolic autoregulation since ethanol produced a decrease in the oxygen consumption of the heart (2.19 +/- 0.43 to 1.62 +/- 0.31 cm3 . min-1 . 100 g-1, P less than 0.05). It was not caused, either, by a decrease in extravascular compression since ethanol did not produce any further decrease in perfusion pressure after maximal dilatation of the coronaries with dipyridamole. In experiments performed either at constant coronary flow or at constant perfusion pressure, flow across the left ventricular wall was redistributed towards the subendocardium during the vasodilatory effect of ethanol. Since in our experimental conditions, changes in the neurohumoral, metabolic and cardiac mechanical factors that influence coronary flow were discarded, this study demonstrates a direct vasodilatory effect of ethanol on the coronary vessels with a redistribution of flow towards the subendocardium.