50DIABETIC a b u t 40% by 0.1 M NaCl but not by even higher concentrations of KCl. Probably Na+, and not a n impurity in the NaCl used, prvp duced the inhilbition because NaCl from a second source gave the same results, and in addition, rates of hydrolysis when using a buffer made from the mono-and dipotassium phosphates were double those found when using a buffer made from the corresponding sodium phosphates. No evidence was found that Na+ inhi'bited, not thrombin, but a contaminant in the 4 thrombin preparations tested. Increasing concentrations of glycerol in the tests produced increasing inhibition of hydrolysis, but the percenltage inhibition due
RAT HEARTto Na+ remained constant. Incubating thornbin at 37" and pH 3.4 gradually destroyed its ability to hydrolyze TAME, but at all times tested the percentage inhibition due to Na+ remained constant. SBTI did not inhibit the rates, and the percentage inhibition by Na+ was the same in the presence and in the absence of SBTI. For these reasons it was concluded that thrombin itself is inhibited by N a f .An impressive body of evidence has accumulated indicating that both cardiac metabolism and cardiac contractile activity rely preferentially on noncarbohydrate sources of energy. That fatty acid metabolism is most closely linked with such energy demands has been indiated in many studies mrried out on mammalian hearts both a t rest and during exercise, employing in vitro and in vivo techniques (1-6).Elevated cardiac glycogen levels in rats resulting from feeding free fatty acids (7,8), during fasting ( 9 ) , and in diabetes (8,lO) have (been abserved; the need for adequate cilrculating growth #hormone far such a polysaccharide increase during fasting has been well defined (9,ll). Not all studies, however, have divorced plasma ketone levels from plasma glucose levels as possible influencing factvrs in regulating cardiac glycogen concentrations. Furthermore, the observation that the dizbetic rat hypophysis con'tains one sixth the normal amount of growth hormone ( 12,