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In the hypoxic myocardium the high energy phosphate content decreases to a critical point at a time when the tissue is susceptible to lactic acidosis and the Ca++ equilibrium is disturbed. The present experimental studies show a direct relationship between the metabolic alteration and the metabolic processes in the high energy phosphate metabolism during and after ischaemia. The reduced affinity of the phosphatase for calcium as well as the reduced Ca++ accumulation in the sarcoplasmic reticulum indicate an inhibition of the ATPase. The decrease of the elevated ATPase activity during the first minutes of reperfusion shows that the block in the operation of the ATPase is not of metabolic nature. The hypothesis is presented that the energy-dependent Ca++ accumulation of the myocardium and particularly its accumulation during ischaemia is an important factor in cardiac tolerance.Assembly of the human peroxisomal trihydroxycoprostan