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Am J Physiol Heart Circ Physiol (March 25, 2004). doi:10.1152/ajpheart.01171.2003
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Submitted on December 9, 2003
Accepted on March 18, 2004

Delta-Opioid Receptor Agonist Reduces the Severity of Post-resuscitation Myocardial Dysfunction

Shijie Sun1*, Max Harry Weil1, Wanchun Tang1, Takashi Kamohara2, and Kada Klouche2

1 Institute of Critical Care Medicine, Palm Springs, CA, USA; Keck School of Medicine, University of Southern California, Los Angeles, CA, USA
2 Institute of Critical Care Medicine, Palm Springs, CA, USA

* To whom correspondence should be addressed. E-mail: drsheart{at}aol.com.

Post-resuscitation myocardial dysfunction is recognized as a leading cause of early death following initially successful cardiopulmonary resuscitation (CPR). In the present study, we hypothesized that a {delta}-opioid receptor agonist would decrease the severity of post-resuscitation myocardial dysfunction and improve survival. Fifteen Sprague-Dawley rats, fasted overnight with access to water, were anesthetized by an intraperitoneal injection of 45 mg/kg pentobarbital sodium. Additional doses of 10 mg/kg were administered at hourly intervals but not within 30 minutes preceding induced ventricular fibrillation (VF). Either the {delta}-opioid receptor agonist, pentazocine (300 µg/kg), pentazocine pre-treated with opioid receptor blocking agent, naloxone (1 mg/kg) or saline placebo was injected into the right atrium after 5 minutes of untreated VF and 3 minutes prior to starting CPR. After an additional 8 minutes of CPR, defibrillation was attempted. All animals were successfully resuscitated. Left ventricular dP/dt40 and cardiac index (CI) were significantly improved in pentazocine-treated animals with significantly longer survival (60±11 vs 16±7 hours, P<0.01). Except for easy of defibrillation, the benefit effects of pentazocine were completely abolished by pre-treatment of naloxone. The concept of pharmacological hibernation employing a {delta}-opioid receptor agonist is a novel and promising intervention for minimizing global ischemic injury during CPR and post-resuscitation myocardial dysfunction.




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