[Prevention of arrhythmogenic and contractile effects of excessive Ca2+ on the heart through adaptation to stress by increasing the activity of sarcoplasmic reticulum].

The experiments with rat isolated hearts and papillary muscles showed that adaptation to short-term stresses increased myocardial resistance to arrhythmogenic and contractile effects of excessive Ca2+. Adaptation caused a three- and fivefold reduction in the contracture and premature beats, respectively, while Ca2+ levels were increased from 1.36 to 10 mM. In the experiments with papillary muscles, the adaptation showed a 6.5-fold decrease in the contracture and significantly limited resting potential depression resulted from lower Na+ concentrations (up to 9 mM) in the perfusion solution. The adaptation to stresses was found to restrict depression of cardiomyocyte electrophysiological parameters that was due to high Ca2+ levels and high heart rate. With the factors, the resting potential in adaptation proved to be significantly higher than in controls and the time of action potential was twice as such as in controls. Biochemical studies demonstrated that Ca2+ transport rates in the sarcoplasmic reticulum, cardiomyocytes of adapted animals were increased by more than 30% whereas the sarcoplasmic reticulum of the heart was more resistant to the effects of endogenous factors of degradation. The authors also discuss a possible mechanism of the cardioprotective effects of adaptation to stress undamaging exposures, which is associated with limited depression of electrophysiological parameters on pathological exposures and with increased Ca2+-transporting capacity of the sarcoplasmic reticulum.