TEMPERATURE, CONTRACTILITY AND HIGH-ENERGY PHOSPHATES IN ANOXIC FISH HEART-MUSCLE

Isolated, electrically paced ventricular tissue of rainbow trout, Oncorhynchus mykiss, was examined at 20 and 10-degrees-C for the effects of different metabolic inhibitions on isometric force development and cellular content of phosphocreatine, creatine, ATP, ADP and AMP. At 20 relative to 10-degrees-C, twitch force was the same, but both twitch development and relaxation occurred over a shorter time and at a considerably higher maximal rate. Inhibition of cellular respiration caused twitch force and phosphocreatine to decrease, both about twice as fast at 20 as at 10-degrees-C. This doubling of energy degradation, i.e. in decrease of phosphocreatine, ATP, and loss of twitch force also occurred in preparations in which the energy liberation was totally blocked by iodoacetate in combination with N2 and cyanide; both anaerobic energy degradation and anaerobic energy liberation expressed as lactate production were doubled. The similar effect of temperature on degradation and liberation of energy might explain why loss of twitch force during a 1-h period of anoxia was the same at both temperatures. The latter result was also found in the myocardium of eel Anguilla anguilla. In spite of its large influence on the time-course of twitch force development, the difference in temperature had no evident effects on the relationship between twitch force and phosphocreatine.