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CARDIOVASCULAR ANESTHESIA

Propofol-Induced Alterations in Myocardial ß-Adrenoceptor Binding and Responsiveness

Weiguo Zhou, MD^*, H. Jerrel Fontenot, MD, PhD^*, Shi-Nan Wang, MD, and Richard H. Kennedy, PhD^*,,

Departments of *Anesthesiology, Pharmacology & Toxicology, and Pharmaceutical Sciences, University of Arkansas for Medical Sciences, Little Rock, Arkansas

Address correspondence and reprint requests to Richard H. Kennedy, PhD, Department of Pharmaceutical Sciences, University of Arkansas for Medical Sciences, 4301 West Markham St., Slot# 522, Little Rock, AR 72205. Address e-mail to kennedyrichardh{at}exchange.uams.edu

Propofol (iv) depresses cardiovascular function in both humans and animals. However, the mechanism underlying this action has not been well described. The present study was designed to test the hypothesis that this effect of propofol results in part from an antagonism of adrenergic control of the heart. Experiments examined effects of propofol on: 1) [³H]CGP12177 (a ß-adrenoceptor antagonist) binding in rat myocardial membranes; and 2) the inotropic and chronotropic actions of isoproterenol in rat left atrial muscle and right atria, respectively. Propofol (25–200 µM) increased the apparent dissociation constant for [³H]CGP12177 without affecting binding site density. Similarly, 200 µM propofol increased the 50% effective concentration values for the dose-dependent positive chronotropic and inotropic actions of isoproterenol in right and left atria, and depressed the maximum increase in spontaneous rate elicited by this ß-adrenoceptor agonist. Other experiments demonstrated that propofol does not alter muscarinic receptor binding as monitored using [³H]quinuclidinylbenzilate. In conclusion, these results indicate that propofol can decrease cardiac ß-adrenoceptor responsiveness; however, the concentrations of propofol required suggest that this action contributes to the cardiovascular depression produced by this anesthetic only during large-dose bolus injection.

Implications: Experiments in membranes and cardiac preparations isolated from rat heart demonstrate that relatively high concentrations of propofol (25–200 µM) are required to antagonize ß-adrenoceptor binding and tissue responsiveness.

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Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999