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Ann Thorac Surg 1999;67:1053-1058
© 1999 The Society of Thoracic Surgeons
a Division of Cardiovascular and Thoracic Surgery, Department of Surgery, Duke University Medical Center, Durham, North Carolina, USA
Accepted for publication October 6, 1998.
Address reprint requests to Dr Chen, Department of Surgery, University of California, San Francisco, Box 0470, S343, San Francisco, CA 94131
e-mail: epchen{at}itsa.ucsf.edu
Background. Chronic 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.
Methods. Animals 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 
1- and ß-adrenergic receptor density and adenylate cyclase activity.
Results. Eight 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 1- and ß-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.
Conclusions. These 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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