[Compensatory factors in acute failure of the isolated heart]

The cardiac output of isolated guinea-pig hearts fell during progressive infusion of Ca2+-complexon, EGTA, or oxidative phosphorylation inhibitor dinitrophenol. Moderate doses of EGTA (0.3-0.6 mM) caused an apparent diminution of the left-ventricular +dP/dt and aortic pressure amplitude but did not influence cardiac output, which was maintained due to a prolongation of the contraction time. When the left-atrial cavity was greatly reduced by ligation, cardiac output fell by 40 per cent while left-ventricular systolic pressure and +dP/dt remained unchanged. In these conditions, EGTA in the same concentration reduced cardiac output by 30 per cent thus proving the important role of the left atrium in the compensation of hypocalcemic heart failure. On the contrary, the infusion of dinitrophenol shortened contraction time and increased myocardial rigidity. The latter change facilitated force development thus contributing to a lesser fall of +dP/dt and aortic pressure amplitude at equal diminution of cardiac output as compared to EGTA action. However, this compensation required a higher elevation of the filling pressure for inflow maintenance.