Abstract

Using the isolated perfused rabbit heart, concomitant changes in coronary inflow and heart action (amplitude and rate) have been recorded. Effects of (a) potassium or calcium chloride injections during normal Locke's perfusion; (b) changing the perfusing fluid to Locke's containing either increased or decreased concentrations of these ions; and (c) the influence of these later changes upon the responses to epinephrine and norepinephrine, were investigated.

It was observed that injections of either potassium or calcium induce coronary dilatation. However, in the case of potassium this is associated with depression of the heart action, while in the case of calcium the effect is associated with stimulation. Neither ion affected heart rate significantly Excess doses of potassium can also induce a paradoxical initial coronary constriction Perfusions with either excess potassium (within limits) or calcium lead to coronary dilatation associated with some cardiac stimulation. In the potassium experiments, responses to both epinephrine and norepinephrine appear to be potentiated but no arrhythmias occur, while in the calcium experiments more or less prolonged ventricular irregularities developed.

During perfusions with relative (50 per cent to 75 per cent) decreases or complete omissions of calcium or potassium ions, coronary dilatation followed in some cases by constriction occurred. In the calcium-deficient experiments, rhythmic heart contractions were maintained for thirty to forty minutes, and characteristic epinephrine and norepinephrine responses were observed, but there were no arrhythmias. Conversely, in the potassium-deficient experiments, the heart contractions were stimulated and with potassium-free perfusions ventricular tachycardia and spontaneous fibrillatory movements ensued The sensitivity to epinephrine or norepinephrine arrhythmias was greatly enhanced by potassium deficiency.

The possible significance of these findings is discussed, and it is concluded that, apart from the mechanical influences associated with changes in the heart contractions, the rate of coronary flow can be strikingly influenced by changes in potassium/calcium ratios in the perfusing fluids; and, both the coronary dilatation and cardiac stimulation induced by epinephrine and norepinephrine can be potentiated by such changes. Since under all conditions of decreased potassium concentrations ventricular arrhythmias were more readily precipitated by epinephrine and norepinephrine, it is postulated that the cardiac effects of these agents might be initiated by some mechanism or mechanisms involving a "potassium -deficit" in the heart.