Electrical and mechanical effects induced by cold temperatures in the ventricle of isolated Rana ridibunda hearts

A temperature decrease changes the contractility of the amphibian heart, but the underlying mechanisms are not totally understood. The objectives of the present work were to better understand the intrinsic mechanisms supporting contractility changes induced by a rapid temperature decrease in the ventricle of Rana ridibunda, and to investigate how fast they develop. Ventricular mechanical cycles (VMCs) and monophasic action potentials (MAPs) recorded from 15 isolated hearts were measured at 15, 30, 45, 60, 90, 120 and 150 s after the application of Ringer solutions of 20, 10 and 5 °C. Treatment with 10 and 5 °C Ringer solutions decreased the heart rate, and increased the magnitude of the ventricular contraction and the duration of the contraction and relaxation periods. The electrical changes included prolongation of the MAP depolarization plateau, which also decreased in amplitude as an effect of perfusion with 5 °C Ringer solution. In addition, treatment with 5 °C Ringer solution increased the latency of contraction. The block of L-type channels totally abolished the depolarization plateau at all perfusion temperatures, but failed to inhibit ventricular contraction. In conclusion, treatment with cold temperatures changes the electrical activity of the ventricular myocardium in R. ridibunda hearts, which results in modified ventricular contractility. Data suggest that in addition to L-type Ca2+ channels, other components that support calcium elevation are present R. ridibunda ventricular cells.