Adverse hemodynamic and ultrastructural changes in dog hearts subjected to protein-calorie malnutrition.

In the absence of thiamine deficiency, the specific effects of protein-calorie malnutrition on left ventricular (L.V.) function are unknown. Mature beagle dogs of both sexes were subjected to a hypocaloric, nitrogen-poor diet which resulted in a weight loss of approximately 40% after seven weeks. Following preparation of this nutritional model, myocardial contractility was assessed acutely by obtaining isovolumetric L.V. contractions on cardiopulmonary bypass at constant heart rate, mean aortic pressure, and at a wide range of end-diastolic volumes. These changes were compared to a matched group of animals which were normally fed. There were consistent decreases in L.V. compliance in malnourished animals compared with normals; indices of ventricular contractility per se (L.V. dp/dt, force-velocity relations, peak developed L.V. pressure) were also diminished in the experimental animals. Myocardial concentration of glycogen was diminished in malnourished compared to control animals. Light and electron microscopic examination confirmed the presence of myofibrillar atrophy in the presence of interstitial edema. These results suggest that protein-calorie malnutrition seriously interferes with normal L.V. function in the experimental animal by reducing compliance as a result of "starvation edema," and by reducing myocardial contractility associated with atrophy of the myofibers.