Cardiomegaly in chronic anemia in ratsman experimental study including ultrastructural, histometric, and stereologic observations.

Postweanling rats maintained on a milk-sugar diet develop a sideropenic anemia, the hemoglobin values falling to less than 30 per cent within 8 to 10 weeks. In that period the heart weight increases by more than 3 times, both ventricles enlarging proportionately. As in other forms of cardiac hypertrophy, a progressive increase in the numbers of connective tissue cells occurs. Ultrastructural and stereologic studies show an appreciable proliferation of the mitochondrial mass in myocardial cells, the mitochondrial fractional volume increasing from a normal of 0.38 to 0.48 per unit cell volume. This quantitative increase is accompanied by a progressive deterioration of the internal cristal structure and the appearance of abnormal, degenerating, and necrotic forms of mitochondria as congestive cardiac failure develops. Myofibrils remain normal. The heart of an anemic rat subjected to an additional workload produced by subdiaphragmatic aortic constriction shows an earlier deterioration of the mitochondrial ultrastructure and stereologic profiles. However, it does not become as large as the heart of the purely anemic animal. In anemic animals with an increased workload, the myofibrillar fractional volume increases from a normal of 0.52 to 0.57 per unit cell volume initially. The active sarcomerogenesis is achieved by Z-band proliferation, which was not observed in the heart of the purely anemic animal. These findings provide a structural basis for the functional and biochemical cardiac deterioration observed in the cardiomegaly induced by chronic anemia.