Positive inotropism in hypothermia partially depends on an increase in maximal Ca²⁺-activated force

We investigated the contribution of maximal Ca²⁺-activated force to the positive inotropism induced by mild hypothermia. Phosphorus-31 nuclear magnetic resonance spectroscopy revealed that neither energy-related phosphorus compounds in myocardium nor intracellular pH was responsible for the change in contractility. Maximal Ca²⁺-activated pressure (MCAP), the intact-heart correlate of maximal Ca²⁺-activated force, was determined in isolated perfused rabbit hearts by measuring isovolumic left ventricular pressure during tetani at extracellular Ca²⁺ concentrations ≥ 10 mM. Tetani were elicited by rapid pacing after exposure to ryanodine. MCAP increased by 2.17 ± 0.28% (means ± SE, P < 0.001, n = 19) for each degree of myocardial cooling between 30 and 38°C. Our results indicate that a primary change in myofilament Ca²⁺ responsiveness underlies the positive inotropism in hypothermia. The increase in maximal Ca²⁺-activated force may explain the observation of positive inotropism without an upward shift in the relation between oxygen consumption and pressure-volume area, as previously reported for cooled whole hearts.