Mildronate [3-(2,2,2-trimethylhydrazinium)propionate dihydrate] ameliorates cardiac function during ischemia by modulating myocardial energy metabolism. Biochemical and pharmacological evidence supports the hypothesis that the mechanism of action of mildronate is based on its regulatory effect on carnitine concentration, whereby mildronate treatment shifts the myocardial energy metabolism from fatty acid oxidation to the more favorable glucose oxidation under ischemic conditions. Because mildronate treatment prepares cellular metabolism and membrane structures to survive ischemic stress conditions, it is possible that mildronate could be regarded as an agent of pharmacological preconditioning.