In an experimental study on isolated isovolumetric guinea-pig hearts, a 2.2-fold reduction of the coronary duct combined with metabolic block caused by dinitrophenol (0.05 mM) resulted in an eleven-fold drop in the attained pressure, and a shorter electric systole, a smaller P wave, and an ST displacement on the ECG. Deep suppression of mechanical and electric activity was combined with reduced glycogen content, and greater K+ and Na+ withdrawal from the heart. Quantitatively, the drop in contractility correlated with K+ withdrawal and ST displacement. A sudden increase in coronary perfusion rate was accompanied by a rapid increase in the rate of K+ elimination from the heart which was proportionate to the rate of hyperfusion, with a simultaneous transitory rise in attained pressure, a great increment in diastolic pressure and the emergence of arrhythmia and fibrillation, the severity of the changes correlating with the degree of K+ loss. A moderate increase in K+ concentration of the perfusate prevented the development of fibrillation and drastically reduced the degree of contracture and glycogen drop during hyperfusion. The obtained results suggest that moderate accumulation of extracellular K+ during the early phase of energy generation disorder can be of a protective nature, as it contributes to a sharp reduction in contractility and energy spending to improve cell survivability in critical conditions.