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J Thorac Cardiovasc Surg 2001;122:476-481
© 2001 The American Association for Thoracic Surgery

Cardiopulmonary Support and Physiology (CPS)

Opioids confer myocardial tolerance to ischemia: Interaction of delta opioid agonists and antagonists

From the Section of Cardiac Surgery, University of Michigan, Ann Arbor, Mich,^a the Department of Pathology, University of Kentucky, Lexington, Ky,^b and the National Institute of Drug Abuse, Bethesda, Md.^c

This work was supported in part by a grant from the American Heart Association, No. 95008730, and National Heart, Lung, and Blood Institute grant HL58781-01A1. Dr Badhwar is The University of Michigan Heart Failure Fellow and is supported in part by a Postdoctoral Fellowship grant from the Canadian Institutes of Health and Research.

Received for publication June 21, 2000. Revisions requested Aug 22, 2000; revisions received Feb 2, 2001. Accepted for publication Feb 20, 2001. Address for reprints: Steven F. Bolling, MD, The University of Michigan Hospitals, Section of Cardiac Surgery, 1500 E Medical Center Dr, 2120D Taubman Center, Box 0348, Ann Arbor, MI 48109-0348 (E-mail: sbolling{at}med.umich.edu).

Abstract

Background: Mammalian hibernation biology is now known to be mediated by delta opioids. The altered myocellular physiology of hibernation closely parallels that of hypothermic ischemia used to protect the heart for cardiac surgery.
Methods and Results: The present study examined the interaction of delta opioid agonists and antagonists on myocardial tolerance to ischemia. By means of a nonhibernating isolated rabbit heart model, functional and metabolic myocardial parameters were assessed during nonischemic baseline and postischemic recovery periods. Control hearts with standard cardioplegic protection alone were compared with those with cardioplegia plus preperfusion with a delta opioid agonist, a delta opioid antagonist, or both. All hearts were then subjected to 2 hours of global ischemia. Compared with cardioplegia alone, postischemic left ventricular developed pressure, coronary flows, and myocardial oxygen consumption were all increased with administration of delta opioid agonists and decreased below baseline with delta opioid antagonists. Functional recovery of left ventricular developed pressure was improved with opioids (control hearts: 36 ± 3 mm Hg vs hearts with cardioplegia plus delta opioid agonist: 65 ± 5 mm Hg, P < .01) and inhibited with antagonists (control hearts: 36 ± 3 mm Hg vs hearts with cardioplegia plus delta opioid antagonist: 17 ± 5 mm Hg, P < .05), and true to form, the protective opioid effect was negated when combined with an antagonist (control hearts: 36 ± 3 mm Hg vs hearts with cardioplegia plus delta opioid agonist and delta opioid antagonist: 42 ± 4 mm Hg, P = not significant).
Conclusions: This study demonstrates that cardiac tolerance to ischemia may be mediated by delta opioids.

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