Volume densities of mitochondria, myofibrils, and unspecified cytoplasm were measured by ultrastructural morphometry in myocardium from dogs, rats, hamsters, mice, and in biopsied tissue from human hearts. Human myocardium was composed of 23% mitochondria, 59% myofibrils, and 18% cytoplasm. Volume densities for mitochondria were 22% for dogs, 28% for rats and hamsters, and 32% for mice. Myofibrillar volume densities were highest in dogs with 63%, 57% for rats and hamsters, and 49% for mice. Differences were significant between all except man and dog, and rat and hamster. In an extensive analysis of canine myocardium, it could be shown that the quantitative composition of tissue from the left ventricular free wall (anterior, lateral, posterior) and the papillary muscles was identical. There were also no differences between subepi- and subendocardium as well as the midmyocardium. Volume densities from longitudinal sections were identical to those from transversal sections. Fixation with glutaraldehyde by perfusion or immersion provided identical results. There were no differences between volume densities in samples from the left ventricular free wall (anterior, lateral, and posterior) in rats, hamsters, and mice. It is concluded that each mammalian species is characterized by a very typical quantitative composition of the myocardium. The increase in mitochondrial volume correlated well with the increase in heart rate and oxygen consumption in smaller animals. These quantitative data are regarded as the morphological correlate of the differing functional capacity of hearts from different species.
The objective of this study was to test the hypothesis that excessive severity of ischaemic heart disease in diabetics is due, in part, to capillary inadequacy. Sections from autopsied hearts of diabetic patients with and without myocardial infarction as well as from those of patients with infarcts and no diabetes were used for morphometric studies of intramural microvessels in areas without infarction. Normoglycaemic patients with normal hearts were also examined. Two to five transverse sections from each of 44 hearts (stained with methenamine silver) were examined for capillary numerical density, capillary to myofibre ratios, and myofibre diameters. Averages for each case and totals for each group were calculated and compared. Normoglycaemic patients with infarcts had increased morphometric values. Diabetics with infarcts had significantly lower capillary densities than the other groups. In conclusion, it is suggested that in diabetes there is an inadequate ischaemia-induced, reactive angiogenesis. This may contribute towards increased myocardial vulnerability in further ischaemic injury and perhaps to diabetic cardiomyopathy.
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