• E P Chen, S A Akhter, H B Bittner, W J Koch, R D Davis, and P Van Trigt.
• Department of Surgery, Duke University Medical Center, Durham, North Carolina, USA. epchen@itsa.ucsf.edu
• Ann. Thorac. Surg. 1999 Apr 1; 67 (4): 1053-8.

BackgroundChronic pulmonary hypertension can lead to compensatory changes in the right ventricle. In this study, the adaptive mechanisms of the right ventricle in the setting of pulmonary hypertension were assessed at the molecular and functional level using a canine model of monocrotaline pyrrole-induced pulmonary hypertension.MethodsAnimals underwent pulmonary artery catheterization to measure pulmonary hemodynamics before and 8 weeks after an injection of monocrotaline pyrrole, 3 mg/kg (n = 8) or placebo (n = 8) (controls). Systolic function was assessed with load-insensitive means (preload-recruitable stroke work). Myocardial biopsy specimens were collected to analyze membrane alpha1- and beta-adrenergic receptor density and adenylate cyclase activity.ResultsEight weeks after injection, significant increases in pulmonary hemodynamic indices were noted in monocrotaline-injected dogs. Significant increases in right ventricular preload-recruitable stroke work were also observed in these animals compared with controls and occurred in association with significant increases in right ventricular alpha1- and beta-adrenergic receptor density and isoproterenol hydrochloride-stimulated adenylate cyclase activity. No significant differences in basal adenylate cyclase activity in the right ventricle were noted between the two groups.ConclusionsThese data suggest that alterations in right ventricular function in the setting of chronic pulmonary hypertension may partially be due to changes in myocardial adrenergic receptor signaling.

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