Temperature dependence of myofilament Ca sensitivity of rat, guinea pig, and frog ventricular muscle

Cooling the superfusate of intact ventricular muscle, from 30°C to below 4°C in < 2 s, leads to contractures thought to reflect the amount of Ca available for release from the sarcoplasmic reticulum (SR). On rewarming, tension transiently increases in guinea pig and rat ventricular muscle. It has been proposed that this rewarming tension spike reflects changes in myofilament Ca sensitivity and maximum Ca-activated force (C(max)) associated with rewarming. There are differences in intracellular Ca regulation among cardiac muscle preparations. Some characteristics of rapid-cooling contractures (e.g., the magnitude of the rewarming spike) also differ between species. Therefore, the Ca sensitivity of skinned ventricular muscle from the rat, guinea pig, and frog was determined at 29 (22°C for frog ventricular preparations), 8, and 1°C. The results show that cooling rat and guinea pig ventricular muscle from 29 to 1°C shifts the pCa vs. tension relationship toward higher [Ca²⁺] by 0.65 and 0.55 pCa units, respectively. Cooling to 1°C also reduced C(max) to 3.3 and 7.8% of that at 29°C in rat and guinea pig ventricular muscle, respectively. Similar results were found for frog ventricular muscle, in which cooling from 22 to 1°C reduced Ca sensitivity by 0.6 pCa units and C(max) to 45.7% of its value at 22°C. However, the degree to which C(max) is depressed at 1°C in rat and guinea pig skinned ventricular muscle is much greater than would be expected from the magnitude of rapid-cooling contractures in these tissues (which are > 4 times the C(max) measured in skinned fibers at 1°C). This suggests that at low temperatures, there is some reversible inhibition of force generation in skinned fibers from rat and guinea pig ventricle.