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  • Title: Diffusion distances, total capillary length and mitochondrial volume in pressure-overload myocardial hypertrophy.
    Author: Kayar SR, Weiss HR.
    Journal: J Mol Cell Cardiol; 1992 Oct; 24(10):1155-66. PubMed ID: 1479616.
    Abstract:
    We examined the relationships between blood pressure, coronary blood flow, cardiac output, myofiber growth, capillarity, mitochondrial content, and capillary and mitochondrial distributions in a pressure-overload model of myocardial hypertrophy. The Goldblatt one kidney-one clip (1K1C) procedure was performed on seven adult rabbits. After 1 month, mean blood pressure increased 50% and mean heart mass increased 30%. Coronary blood flow and cardiac output at rest were similar in control and 1K1C hearts; cardiac output fell 40% when 1K1C hearts were paced to 35% above basal heart rate. Capillary density in the left ventricular free wall (LV) decreased with increasing fiber size by as much as 30%. However, capillary-to-fiber ratio and total capillary length in the LV increased with heart size by up to 30% and 80%, respectively. This indicated that there was some proliferation of capillaries taking place, but not enough in comparison to fiber growth to prevent the lengthening of distances between capillaries. Mitochondrial volume density decreased by as much as 30% with increasing heart size, but total mitochondrial volume increased up to 80%. This indicated that there was some proliferation of mitochondria, but not enough to prevent dilution of mitochondria by the growing myofibrillar elements. Analysis of the distribution of mitochondria suggested that the new mitochondrial material was added to the center of myofibers, thereby further lengthening oxygen diffusion distances. There was a constant ratio of 10.4 +/- 0.3 km of capillaries per ml of mitochondria in 1K1C and control hearts, demonstrating that the structures for oxygen supply and consumption were remaining in fixed proportion to each other. There was no evidence that the decreased performance of paced 1K1C hearts was attributable to an oxygen diffusion limitation to mitochondria.
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