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The hexose monophosphate shunt activity as well as the non-oxidative pentose pathway in nucleic acids synthesis was studied in the time course of the left ventricular hypertrophy of 63 male rats weighing 200 to 600 Gm. induced by cellophane perinephritis hypertension. Another 26 rats with same range of body weight were employed as control group.(1) Ventricular hypertrophy was estimated by the ratio of the ventricular weight to body weight, and it revealed an apparent increase of the ratio in only left ventricle ranging all body weights from 4 to 34 weeks after operation.(2) Left heart failure was not demonstrated by determination of the water content in lungs in this series of experiment.(3) At the early stage of the left ventricular overload, total DNA content decreased, however, during continuous overload total DNA content returned to normal, and then, at the late stage of compensated hypertrophy or of this series, this value increased over normal level. This fact suggests the possibility of cellular damage at early stage and cellular hyperplasia at late stage of ventricular overload. The incorporation ratio of C14glucose into DNA increased tremendously at 4 weeks after operation, which was likely an increase in degradation and synthesis of DNA. The HMP shunt activity in DNA synthesis was not detected in all course of ventricular overload.(4) RNA content increased through all course of experiment, however, the incorporation of C14-glucose into RNA increased rapidly at early stage of overload, and then returned to normal level during compensatory hypertrophy, and finally came down under normal level at late stage of compensatory hypertrophy. The HMP shunt activity in RNA synthesis was tremendously activated at early stage of ventricular overload, but disappeared even in the compensatory hypertrophy. Therefore, the HMP shunt may be considered to play some important roles in occurrence of cardiac hypertrophy and even cardiac failure.

Nucleic Acid Metabolism and Depression of Hexosemonophosphate Pathway in Experimental Cardiac Hypertrophy