Abstract
Although variations in temperature have a profound impact on cardiac function, little is known regarding the excitation and contractile parameters over a broad temperature interval. In view of the clinical implications of lowered temperature in resuscitation and in cardiac preservation/evaluation for transplantation, we have examined the contractile function using Langendorff perfused hearts and isolated trabecular muscle from pig, in combination with electrophysiology and x-ray diffraction. Lowered temperature in the range 37°C-22°C was associated with an increase in systolic pressure and active force. In permeabilized preparations, force and Ca(2+) sensitivity decreased with temperature, showing that the increased force down to 22°C in the intact heart and trabeculae was not due to changes in thin filament regulation, but most likely to increased activator [Ca(2+)]. At lower temperature (<22°C), force of the heart decreased, suggesting that the temperature effects in the regulatory system became dominating. ECG analysis showed that frequency was lowered and that PQ-, QS- and QT- times were prolonged at lower temperature. This was associated with a gradual depolarization of the cell membrane, prolonged action potential and an attenuation of the fast upstroke phase. These changes in rise time and amplitude of the action potential would predispose for uneven propagation and arrhythmia as temperature is lowered. At the same time, the prolonged action potential can be associated with an increased [Ca(2+)] at lower temperature. Small angle x-ray diffraction showed that the filament lattice of intact trabecular muscle tended to swell at low temperature (10°C vs. 22°C) and revealed a mass transfer from myosin to actin filaments, which would reflect changes in cellular physiology and contractile system structure at low temperature.