Experiments on noninbred albino male rats under the conditions of the whole body and the isolated isovolumically contracting heart have shown that a substantial contribution to postresuscitative cardiac damages is made by energy deficiency that triggers a group of mechanisms of damaging cardiomyocytic membranes. Exogenous creatine phosphate (CP) reduces postresuscitative mortality rates, improves bioenergy, contractile and rhythmical functions of the heart, decreases the rate of myocardial lipid peroxidation, by showing as a whole a cardioprotective action. The latter is realized by directly protecting the cardiomyocytic sarcolemma and the improvement of energy metabolism is secondary. Despite the likely mediation of this effect, improved energy metabolism is undoubtedly a key point of the protective action of exogenous CP if the heart is postresuscitatively damaged.