The Effect of Chronic Protein-Calorie Undernutrition in the Rat on Myocardial Function and Cardiac Function

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The effect of chronic protein-calorie undernutrition (PCU) on cardiac structure, biochemistry, myocardial function, and left ventricular dynamics was studied in young, male, Long-Evans rats. Chronic PCU produced marked cachexia of the marasmic type (body weight decreased to 48% of normally nourished control rats) and cardiac atrophy (heart weight at 57% of control). Myocardial structure on light microscopy was normal and myocardial edema (dry/wet weight) was not present. An increased left ventricular DNA content (1.82 + 0.67 BE VS. 1.25 ± 0.58 pg/mg tissue wet weight) and collagen content (70.61 ± 4.54 vs. 31.72 ± 2.44 pg/mg, P< 0.001) in the presence of normal concentrations of RNA and actomyosin suggested a decrease in myofiber size with normal contractile proteins and protein synthesis. Resting length-tension curves for left ventricular papillary muscles failed to demonstrate alterations in myocardial stiffness with PCU. Active length-tension curves demonstrated enhanced myocardial contractility in chronic PCU hearts: peak developed isometric tension at U, was 4.84 ± 0.21 vs. 3.24 ± 0.31 g/mm+, P < 0.01. The in situ heart preparation in anesthetized PCU rats demonstrated bradycardia, hypotension, and a depressed cardiac output when compared to control hearts. However, cardiac output adjusted for body weight was normal (0.048 ± 0.005 vs. 0.044 ± 0.002 ml/min per g), and ventricular function curves, using stroke work index, showed a normal cardiac reserve in PCU rats. We conclude that uncomplicated chronic PCU is accompanied by cardiac atrophy, normal or enhanced myocardial contractility, and left ventricular function that has adjusted to the decrease in body mass and metabolic requirements. Ore Res 45:144-162, 1979

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