A B S T R A C T Passive stiffness and hydroxyproline content of myocardium hypertrophied by pressureloading 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 -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, a and B were determined from the relationship a = a(ee -1) where a = stress and e = Lagrangian strain. Elastic stiffness (dl/dE) was derived from: da/de = f#a + ,3a. Right ventricular hydroxyproline increased in proportion to muscle mass so that hydroxyproline concentration remained unchanged after banding. Both a, f, and elastic stiffnessstress relations were similar to values in nonbanded controls. Thus, we did not observe an increase in passive stiffness or hydroxyproline concentration of pressure-induced hypertrophied myocardium in contrast to most previous studies.

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335cated that the increase in alpha amino nitrogen was due to a generalized failure of the reabsorptive mechanisms rather than inhi bition of a specific transport system for groups of amino acids as described by Beyer( lo).The finding af variable potassium excretion appears to differ from the report by Robin, et aZ.( 11) that hypokalemia occurs during salicylate poisoning. However, this hypokalemia was thought to be a manifestation af the respiratory alkalosis caused by salicylate rather than a specific function of salicylate.Summary. 1. Both small and large amounts of acetylsalicylic acid have a marked inhibitory effect on renal excretion of sodium and chloride. 2. Uricosuric amounts of acetylsalicylic acid block the renal reabsorptive mechanisms for amino acids. 3. The findings of Yu and Gutman concerning the paradoxical effects of salicylate on uric acid excretion are confirmed.

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