On the reversal of the heart hypodynamia by means of a prolonged cooling.

Lizard ventricles induced to hypodynamia by the high flow rate of the perfusing solution were submitted either to brief periods of cooling (from 20 to 25 degrees C), or to a prolonged hypothermic incubation (35 h at 4 degrees C) followed by a recovery at room (20 degrees C) or reduced (15 degrees C) temperature. Isometric rested state contractions as well as staircases and steady-state twitches at 20 or 4 min-1 were recorded. While a brief exposure to reduced temperature proved to increase the peak tension of the twitches, without altering the peculiar tension-frequency relation and the pattern of the staircases which characterize the hypodynamic condition, a transitory post-effect of the prolonged hypothermic incubation was noticed, that causes the reappearance of the contractility features which characterize the normal inotropic state. The results are discussed in the light of the double-component hypothesis for the twitch in lizard ventricular cells, and interpreted as evidences that a brief exposure to low temperatures enhances the transmembrane Ca++ influx during the AP, that causes an augmentation of the late, slow rising component of the twitch; while the prolonged hypothermic incubation would cause also an increase of the Ca++ content in a cellular store, and consequently a potentiation of the early, impulsive component of the twitch.