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J Thorac Cardiovasc Surg 1995;109:236-241
© 1995 Mosby, Inc.

CARDIOPULMONARY BYPASS, MYOCARDIAL MANAGEMENT, AND SUPPORT TECHNIQUES

Marked enhancement in myocardial function resulting from overexpression of a human ß–adrenergic receptor gene

Durham, N.C., La Jolla, Calif., and Houston, Tex.

Sponsored by David C. Sabiston, Jr., MD

Durham, N.C.

Supported in part by National Institutes of Health grants HL-16037 (R.J.l.), 5F32-CA09350 (C.A.M.), HL-18468 (P.C.D.), American Heart Association California Affiliate 92-300 (H.A.R.), and NIA-RO1-AG662 (R.A.B.)

Address for reprints: Robert J. Lefkowitz, MD, Duke University Medical Center, DUMC BOX 3821, Durham, NC 27710.

Abstract

Transgenic mice with intense cardiac expression of humanß-adrenergic receptor gene were engineered and shown to display market improvements in baseline myocardial and left ventricular function. Heart/body weight ratios and histologic appearance were not found to be significantly altered, suggesting that receptor gene expression did not induce pathologic changes. Given the substantial reduction inß-adrenergic receptor density and result reduction in inotropic responsiveness observed in chronic heart failure, these finding represent a novel approach for increasing myocardial function with important clinical implications. (J THORACCARDIOVASCSURG1995;109:236-41)

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