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J Thorac Cardiovasc Surg 2000;120:342-349
© 2000 The American Association for Thoracic Surgery

Surgery for acquired cardiovascular disease

Early effects of right ventricular volume overload on ventricular performance and ß-adrenergic signaling

From the Department of General and Thoracic Surgery, Duke University Medical Center, Durham, NC.

Supported by grants from the National Institutes of Health: HL56227 (D.D.G.), HL56205 (W.J.K.), and HL09907 (A.S.).

Presented in part at the Seventy-first Scientific Sessions of the American Heart Association, November 1998.

Address for reprints: Donald D. Glower, MD, PO Box 3851, Duke University Medical Center, Durham, NC 27710(E-mail: glowe001{at}mc.duke.edu ).

Objective: Right ventricular dysfunction is a poorly understood but persistent clinical problem. This study was undertaken to evaluate ventricular performance and ß-adrenergic receptor signaling in a tricuspid regurgitation model of right ventricular overload.
Methods: Seventeen dogs were chronically instrumented with epicardial dimension transducers. By means of the shell-subtraction model, right ventricular pressure-volume relationships were evaluated in normal and right ventricular overload states. Right ventricular chamber performance was quantified by the stroke work at an end-diastolic volume relationship.
Results: Right ventricular volume overload caused a 28% ± 11% and 31% ± 9% decline in chamber performance acutely and at 1 week, respectively, whereas end-diastolic volume increased from 45 ± 21 to 60 ± 30 mL (P = .019). ß-Adrenergic receptor signaling in myocardial samples was assessed, examining adenylyl cyclase and G-protein–coupled receptor kinase activity. Stimulated adenylyl cyclase activity significantly decreased, and G-protein–coupled receptor kinase activity significantly increased in both left and right ventricular samples caused by increased levels of ß-adrenergic receptor kinase 1. No change in ß-adrenergic receptor density was seen at 1 week.
Conclusions: Early right ventricular overload is associated with impaired right ventricular chamber contractility, dilation, and, importantly, a biventricular alteration of ß-adrenergic receptor signaling.

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