Facilitating effect of cold shock on recovery from anoxia-induced contractile depression in isolated rat heart and heart muscle.

The effect of rapid cooling on the recovery process from anoxia-induced hypodynamic state was studied in isolated rat ventricular muscle and ventricle. Following 10-15 minutes' perfusion of N2-saturated Krebs solution, the muscle was reoxygenated. When the muscle was rapidly cooled for 10-30 seconds during the early phase of reoxygenation, the rate of recovery from contracture significantly increased (p less than 0.01). Rapid cooling was also effective on the recovery from contracture induced by superfusion of Krebs solution with lowered sodium chloride concentration, but it did not affect the recovery from rigor induced by CN-. In the recovery from sustained anoxia (60 minutes), cooling facilitated reattainment of tension development and reduction in contracture tension. Similarly, in whole heart, 2-3 episodes of rapid cooling for about 60 seconds significantly accelerated the recovery of pressure development after 30 minutes of anoxia. At 60 minutes after reoxygenation, pressure development in hearts that were reoxygenated without rapid cooling was 29.8 +/- 26.9% (mean +/- SD) of pressure developed before anoxia. This value increased to 93.8 +/- 27.5% following recurrent rapid cooling (p less than 0.001). At the same time, rapid cooling prevented any significant elevation in resting tension (development of oxygen paradox). These results indicate that excess intracellular calcium ions were removed by rapid cooling. This relief of the myocardium from calcium overload is believed to improve mitochondrial function and result in facilitated recovery of contractile activity.