Effect of temperature on Ca(2+)-dependent and mechanical modulators of relaxation in mammalian myocardium.

Temperature has long been known to affect mammalian cardiac muscle twitch characteristics; duration is prolonged and force is greater at 24 degrees C compared to 37 degrees C. Myocardial relaxation is also influenced by temperature; its time course is governed by a variety of temperature dependent intracellular processes. To investigate the effects of temperature on the interplay between sarcoplasmic reticulum calcium handling and crossbridge cycling as determinants of relaxation time course, we looked at the effects of temperature on load dependence of relaxation (LDoR). Load clamps of amplitude 90%, 80%...10% of peak developed isometric force were recorded at 24 degrees, 30 degrees, and 37 degrees C in rat right ventricular papillary muscles (n = 7), and load dependence of relaxation was analysed. Increasing temperature attenuated LDoR, suggesting there is a decrease in the efficacy of the sarcoplasmic reticulum relative to mechanical determinants of relaxation time course. Therefore, to more directly probe the relative contributions of changes in the [Ca2+]i transient and mechanical determinants of relaxation, we measured T + dF/dt (time to peak +dF/dt) as an indicator of the timing of peak [Ca2+] and tau f (the time constant of the final exponential decay of force from 10% developed force) as an indicator of mechanical kinetics. Both the [Ca2+]i transient and mechanical processes became faster with increasing temperature, as indicated by decreases in T + dF/dt and tau f; however, the ratio T + dF/dt/tau f increased. We interpret the decrease in LDoR and the increase in T + dF/dt/tau f as demonstrating that mechanical kinetics are more sensitive to temperature than is sarcoplasmic reticulum Ca2+ handling.