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J Thorac Cardiovasc Surg 1995;110:746-0751
© 1995 Mosby, Inc.
CARDIAC AND PULMONARY REPLACEMENT |
Durham, N.C.
Supported in part by American Heart Association Grants in Aid No. 92009270 (D. A. S.) and No. 90011230 (P. V. T).
Received for publication Nov. 18, 1994. Accepted for publication Feb. 3, 1995. Address for reprints: Thomas A. D'Amico, MD, Duke University Medical Center, Box 31013, Durham, NC 27710.
Abstract
Brain death often results in a series of hemodynamic alterations that complicate the treatment of potential organ donors before transplantation. The deterioration of myocardial performance after brain death has been described; however, the pathophysiologic process of the myocardial dysfunction that occurs after brain death has not been elucidated. This study was designed to analyze the function of the myocardial ß-adrenergic receptor and the development of left ventricular dysfunction in a porcine model of experimental brain death. Analysis of the ß-receptor included determination of receptor density and adenylate cyclase activity after stimulation independently at the receptor protein, the G protein, and the adenylate cyclase moiety. Myocardial ß-receptor density did not change after the induction of brain death. A decrease in stimulated adenylate cyclase activity was observed within the first hour after brain death at the level of the ß-receptor, the G protein, and the adenylate cyclase moiety, which suggests the occurrence of rapid desensitization of ß-receptor function. Significant deterioration of myocardial performance also occurred within the first hour after brain death, represented by a decrease in preloadrecruitable stroke work compared with the baseline value. The deterioration of myocardial performance after brain death correlates temporally with desensitization of the myocardial ß-receptor signal transduction system. The mechanism of impairment appears to be localized to the adenylate cyclase moiety itself. (J THORACCARDIOVASCSURG95;110: 51)
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