Regional changes in myocyte size and number in propranolol-treated hyperthyroid rats
- PMID: 2961929
Regional changes in myocyte size and number in propranolol-treated hyperthyroid rats
Abstract
The effects of beta-adrenergic blockade and hyperthyroidism on cardiac myocyte structure was examined. Isolated myocytes were prepared from controls and rats treated for 10 weeks with desiccated thyroid hormone (T), propranolol, and desiccated thyroid hormone plus propranolol (TP). Cells were collected from the right and left ventricle. Cell volume was measured with a Coulter Channelyzer system. Cell length was measured directly using a phase microscope. Myocyte cross-sectional area was calculated from cell volume/length. In addition, hearts from animals in each group were perfusion-fixed and myocyte volume percent was determined morphometrically from tissue sections. The number of right and left ventricular myocytes was calculated using data from isolated cells and whole-sectioned tissue. Propranolol normalized heart rate in hyperthyroid rats. Heart weight to body weight ratios were elevated to a similar extent in both T and TP groups. Compared with controls, myocyte volume was increased (p less than 0.01) in each region of T and TP. Right ventricles had a greater degree of myocyte hypertrophy than left ventricles in both rat groups treated with thyroid hormones. Cell length was increased (p less than 0.01) in T and TP. Most of the myocyte hypertrophy, however, was due to an increase in cross-sectional area. Although volume was unchanged with propranolol treatment alone, myocytes from each region had an increase in length (p less than 0.01) and a reduction in cross-sectional area (N.S.). Myocyte number was slightly reduced in each treatment group, but changes were not statistically significant. In conclusion, thyroid hormones stimulate myocyte hypertrophy by increasing both length and cross-sectional area. Propranolol modifies myocyte dimensions in both euthyroid and hyperthyroid rats, but does not prevent thyroid hormone induced cardiac hypertrophy.
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