The effect of chronic protein-calorie undernutrition in the rat on myocardial function and cardiac function.

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Abstract
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 wt decreased to 48% of normally nourished control rats) and cardiac atrophy (heart wt at 57% of control). Myocardial structure on light microscopy was normal and myocardial edema (dry/wet wt) was not present. An increased left ventricular DNA content (1.82 + 0.97 SE vs. 1.25 .+-. 0.58 .mu.g/p tissue wet wt) and collagen content (70.61 .+-. 4.54 vs. 31.72 .+-. 2.44 .mu.g/m P < 0.001) in the presence of normal concentrations of RNA and actomyosin suggested a decrease in myofibril 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 Lmax [maximum length] was 4.84 .+-. 0.21 vs. 3.24 .+-. 0.31 g/mm2, P < 0.01. The in situ heart preparation in anesthetized PCU rats demonstrated bradycardia, hypotension output when compared to control hearts. Cardiac output adjusted for body wt 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. 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.