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Chronic overloading of the rat heart induces a cascade of adaptational events which compensate for the increase in work. Two of these have been extensively described: a qualitative event with an isomyosin change leading to an improved efficiency and a quantitative event resulting in cardiac hypertrophy. By means of immunofluorescence, we investigated if elements of the cytoskeleton, i.e. microtubules and intermediate filaments, could be triggers for these adaptational mechanisms. Studies of overloaded heart were performed in young rats with aortic stenosis or adult rats with aortic insufficiency. Cardiac myocytes were isolated and labelled by immunofluorescence with antibodies raised against V1 or V3 isomyosin, desmin or tubulin. The aim of the work was to visualize: when and where the shift in the expression of isomyosins occurs within the myocytes; the eventual changes in the pattern of intermediate filaments of desmin and/or of microtubules during the adaptation of myocytes to overload. We observed: that the shift from the high (V1) to low (V3) ATPase isomyosin occurred in a population of myocytes soon after stenosis; that changes in the pattern of microtubules occurred soon after induction of hypertrophy; no changes in the distribution or intensity of the staining of desmin.
Rappaport et al. (Sun,) studied this question.