Dinitrophenol (DNP) induces failure of the canine heart-lung-preparation and increases specifically its O2-consumption. Lanatoside C compensates this failure as long as the degree of dinitrophenol poisoning is moderate and the O2-supply sufficiently ample. This cardiac glycoside does not influence the metabolic action of dinitrophenol, i.e. the increased O2-consumption, nor does it counteract the failure due to a large degree of dinitrophenol poisoning. From these findings the mechanism of action of Lanatoside C is discussed.