Myocardial hydroxyproline and mechanical response to prolonged pressure loading followed by unloading in the cat.

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Abstract
To determine the myocardial response to prolonged pressure-loading and unloading, kittens weighing 0.8-1.2 kg underwent pulmonary artery banding, which initially elevated right ventricular (RV) systolic pressure by 10-15 mm Hg. 52 and 76 wk later; RV weight/body weight had increased by approximately 80%. Total RV hydroxyproline had increased significantly, whereas hydroxyproline concentration was unchanged from that of nonbanded animals of comparable age. In isometrically contracting RV papillary muscles, peak active force was significantly less at 76 wk (3.3 +/- 0.8 [SD] g/mm2 than at 52 wk (5.1 +/- 0.8 g/mm2) or in nonbanded animals (4.8 +/- 0.8 g/mm2). Velocity of muscle shortening at comparable loads was unchanged after 52 wk but was significantly less after 76 wk. In nonstimulated, slowly stretched muscles, passive stiffness constants, alpha and beta, derived from delta = alpha(e beta epsilon - 1), where delta is instantaneous stress and epsilon is Lagrangian strain, were unchanged by banding. The band was removed after 52 wk in additional animals that were studied 24 wk later. In those animals with normal RV pressures at death, hypertrophy had regressed and hydroxyproline concentration was comparable to that of nonbanded and banded animals; Active and passive mechanical function remained normal. In this model, changes in hydroxyproline parallel changes in muscle mass, and passive stiffness remains normal during development and regression of hypertrophy. Removal of the pressure load after prolonged hypertrophy prevents or retards the late development of myocardial dysfunction.