Desensitization of myocardial beta-adrenergic receptors and deterioration of left ventricular function after brain death.

Published

Journal Article

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 beta-adrenergic receptor and the development of left ventricular dysfunction in a porcine model of experimental brain death. Analysis of the beta-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 beta-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 beta-receptor, the G protein, and the adenylate cyclase moiety, which suggests the occurrence of rapid desensitization of beta-receptor function. Significant deterioration of myocardial performance also occurred within the first hour after brain death, represented by a decrease in preload-recruitable stroke work compared with the baseline value. The deterioration of myocardial performance after brain death correlates temporally with desensitization of the myocardial beta-receptor signal transduction system. The mechanism of impairment appears to be localized to the adenylate cyclase moiety itself.

Full Text

Duke Authors

Cited Authors

  • D'Amico, TA; Meyers, CH; Koutlas, TC; Peterseim, DS; Sabiston, DC; Van Trigt, P; Schwinn, DA

Published Date

  • September 1995

Published In

Volume / Issue

  • 110 / 3

Start / End Page

  • 746 - 751

PubMed ID

  • 7564442

Pubmed Central ID

  • 7564442

International Standard Serial Number (ISSN)

  • 0022-5223

Digital Object Identifier (DOI)

  • 10.1016/s0022-5223(95)70107-9

Language

  • eng

Conference Location

  • United States