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Does gradual pressure-induced hypertrophy via pulmonary artery banding increase passive stiffness and hydroxyproline concentration in kitten myocardium?
Does gradual pressure-induced hypertrophy via pulmonary artery banding increase passive stiffness and hydroxyproline concentration in kitten myocardium?
In a kitten model of gradually developing pressure-induced right ventricular hypertrophy, neither passive stiffness nor hydroxyproline concentration increased, contrasting with findings in adult models of abrupt pressure overload.
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No stiffness or hydroxyproline rise with gradual kitten banding; challenges abrupt adult overload models and leaves open rate- or age-dependent effects.
Passive stiffness and hydroxyproline content of myocardium hypertrophied by pressure-loading were determined in kittens 2, 8-16, and 24-52 wk after pulmonary artery banding, which initially elevated right ventricular systolic pressure by 10-15 mm Hg. Right ventricular mass increased by approximately 75%, three-quarters of which occurred during the first 2 wk after banding. Passive stiffness was assessed from resting length-tension relations of isometrically contracting isolated right ventricular papillary muscles. Stiffness constants, alpha and beta were determined from the relationship sigma = alpha (e beta epsilon - 1) where sigma = stress and epsilon = Lagrangian strain. Elastic stiffness (d sigma/d epsilon) was derived from: d sigma/d epsilon = beta sigma + beta alpha. Right ventricular hydroxyproline increased in proportion to muscle mass so that hydroxyproline concentration remained unchanged after banding. Both alpha, beta, and elastic stiffness-stress relations were similar to values in nonbanded controls. Thus, we did not observe an increase in passive stiffness or hydroxyproline concentration of pressure-stiffness or hydroxyproline concentration of pressure-induced hypertrophied myocardium in contrast to most previous studies.
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Williams et al. (1982) studied this question.
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