THE purpose of this research was to determine whether or not the heart in the absence of circulating carbohydrate would utilize added amino acids, and to secure further evidence for the direct oxidation of fat by the heart.That ammonia appears in muscle and in fluids by which muscle or organs have been perfused has been demonstrated by many [Warburg, Posner, and Negelein, 1924;Winterstein and Hirschberg, 1925;Embden, 1927;Embden and Schumacher, 1929; Lehnartz, 1929;and Clark, Gaddie and Stewart, 1931]. Meyerhof, Lohmann and Meier [1925] and Reinwein [1928] have stated that with good oxygenation sections of liver, in contrast to muscle, are capable of forming ammonia from amino acids. But when dead or dying tissue is used in thin sections one is confronted with the fact that other than living processes are at work. That the living kidney will produce ammonia has been demonstrated by Nash and Benedict [1921], Gottlieb [1928] and Embden and Schumacher [1929].The work of Krebs [1933] would go to show that the amino acids are deaminated not only in the liver but also in the kidney of the rat and that the formation of ammonia is 3-10 times greater from the non-naturally occurring amino acids than from the natural amino acids. Gyorgy and R6thler [1927] have shown that liver, kidney, thymus and muscle, as well as extracts of these tissues, are capable of forming ammonia from sodium nuclein (Merck) and adenosine under conditions in which for the liver the optimum pH is 5-2-5-5. They also state that, for several kinds of tissue, ammonia arises either from known amino acids by methods in a manner incompatible with the known laws of autolytic production of ammonia in tissues as by enzymes or, and this they regard as certainly unlikely, from protein, urea or by deamination of amino acids during PH. LXXXVI.