POSTREST POTENTIATION AND ITS DECAY AFTER INOTROPIC INTERVENTIONS IN ISOLATED RAT-HEART MUSCLE

The effects of Various inotropic interventions on post-rest potentiati on and its decay were investigated in isolated cardiac muscle. The ino tropic interventions studied were: reduced extracellular Na+ and eleva ted extracellular Ca2+ concentration; exposure to ouabain, monensin, i soprenaline, phenylephrine and cirazoline. Force of contraction (stimu lation frequency 2 Hz) was measured isometrically in left atria and ri ght ventricular strips of rat hearts. Maximum post-rest potentiation w as reached after 10 sec. of rest and amounted to 245+/-26% of pre-rest control in ventricle and 192+/-15% in atria. Ca2+-recirculation fract ion was calculated from the decay of post-rest potentiation after resu mption of regular stimulation, it was 0.77+/-0.01 in 11 control ventri cular strips. High concentrations of caffeine (3 mmol/l) completely ab olished post-rest potentiation in both tissues. The development of pos t-rest potentiation was accelerated in the presence of most of the ino tropic agents. However, with the exception of ouabain and only in atri al muscle, none of the inotropic interventions produced higher post-re st contraction amplitudes than during controls. In rat heart muscle, t he inotropic interventions studied are not any more effective in augme nting force of contraction than prolonged stimulation intervals. This suggests that (1) the distribution of Ca2+ into the sarcoplasmic retic ulum is at a maximum during post-rest potentiation; (2) modifications of signal transduction pathways cannot further increase post-rest pote ntiation; and therefore that (3) shifts in Ca2+ distribution act as a limiting factor.