Isolated frog heart performance after stimulation by adrenaline against the background of new metal-complex antihypoxant πQ1983 action

The dynamic of isolated nonfixed heart bioimpedance changing had been studied in experiments on frogs (Rana temporaria, n = 20) after stimulation by adrenaline and application of the new antihypoxic metal-complex substance πQ1983 just on myocardium. The curve of heart bioimpedance changing (impedancecardiogram) was registered in vitro by the computer reographic apparatus “Reospectr” (Neurosoft, Russia). Simultaneously ECG was registered too. After placing of a heart in condition of the experiment and after placement of all electrodes the stimulation by adrenaline were performed by dropping of 0.1 % adrenaline hydrochloride solution on myocardium (control group). On the hearts of the experimental group were applied the substance πQ1983 solution 15 min before stimulation by adrenaline (experimental group). Was established that substance πQ1983 increases the resistance of frog myocardium to the stimulation by adrenaline in vitro making longer its mechanical and electrical work more than twice. The obtained data confirm presence of soft direct cardiodepressive effect of the substance πQ1983 that supplements the conception of different mechanisms of its antihypoxic impact.

Frog ventricle: participation of SR in excitation-contraction coupling

Activation of the first beat (B1) following a 60-s pause is diminished in isometrically contracting frog ventricular strips, in contrast to the augmentation documented for sarcoplasmic reticulum (SR)-dependent mammalian myocardium. However, treatment of frog ventricular strips with ouabain, an indirect inhibitor of the sarcolemmal Na+-Ca2+ exchanger, selectively enhanced postpause beats suggesting that in the absence of ouabain significant extrusion of cellular Ca2+ occurred during the pause. Because resting tension did not increase during the pause in ouabain-treated strips, the nonextruded Ca2+ must have been sequestered into a compartment such as SR. Steady-state beats were not affected by ouabain; its actions appeared to be separate from its known positive inotropism. Caffeine, a direct SR stimulus, initially enhanced B1 and subsequently decreased activation of all beats, which was consistent with initial augmentation of SR Ca2+ release and subsequent depletion of SR Ca2+ stores. Ouabain both potentiated the stimulatory effects and blocked the inhibitory effects of caffeine, suggesting that ouabain increased Ca2+ stores in the same intracellular Ca2+ pool as that acted on by caffeine, the SR. Ryanodine, an inhibitor of SR in mammalian myocardium, did not affect activation of frog myocardium. SR may be an important site for activator Ca2+ cycling in frog myocardium under control conditions as well as after long diastolic intervals in the presence of ouabain.