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In this paper, an attempt was made to describe the alterations of the myocardial energy metabolism following moderate stenoses of aorta or pulmonary artery. Biochemical investigations regarding the main high energy phosphates and a large series of dehydrogenases in the myocardium of the overloaded ventricles have revealed the following facts: (1) the myocardial CP-CPK system appears to be more labile than the myocardial AMP-ATP system in response to a ventricular overload; (2) the changes in the amounts of myocardial high energy phosphates seem to be more important in the right chronic cardiac overload than in the left one; (3) before the overloaded ventricle becomes insufficient, the myocardial dehydrogenase system elicits no alteration, suggesting that the oxidative phosphorylation is not affected; (4) there is a closer relationship between the coronary flow and pressure and the myocardial energy metabolism than that existing between this metabolism and the tension of the myocardial fibres following a persistent increase in the systemic arterial resistance.

An approach to explain the early metabolic disturbances induced by a moderate ischaemia on the basis of comparative biochemical investigations concerning the oxidative metabolism in the skeletal muscles, is the object of the present paper. These investigations have revealed the following findings: (i) during a slight ischaemia the skeletal muscle maintains its ability to oxidize in vitro lactate and exhibits an increased activity in oxidizing pyruvate, succinate and L-glutamate, and (ii) the stores of adenosine and ATP are depleted and an important accumulation of inorganic phosphate, accompanied by a remarkable activation of phosphatases, occurs in the ischaemic muscle, while no significant changes in the ATPase and creatine phosphokinase activities and in the amount of AMP, ADP and creatine phosphate are detectable in this muscle.