title: delta-Opioid-induced pharmacologic myocardial hibernation during cardiopulmonary resuscitation.
abstract: OBJECTIVE
  Cardiac arrest and cardiopulmonary resuscitation is an event of global myocardial ischemia and reperfusion, which is associated with severe postresuscitation myocardial dysfunction and fatal outcome. Evidence has demonstrated that mammalian hibernation is triggered by cyclic variation of a delta-opiate-like compound in endogenous serum, during which the myocardial metabolism is dramatically reduced and the myocardium tolerates the stress of ischemia and reperfusion without overt ischemic and reperfusion injury. Previous investigations also proved that the delta-opioid agonist elicited the cardioprotection in a model of regional ischemic intact heart or myocyte. Accordingly, we were prompted to search for an alternative intervention of pharmacologically induced myocardial hibernation that would result in rapid reductions of myocardial metabolism and therefore minimize the myocardial ischemic and reperfusion injury during cardiac arrest and cardiopulmonary resuscitation.
  
  
  METHODS
  Prospective, controlled laboratory study.
  
  
  METHODS
  University-affiliated research laboratory.
  
  
  METHODS
  In the series of studies performed in the established rat and pig model of cardiac arrest and cardiopulmonary resuscitation, the delta-opioid receptor agonist, pentazocine, was administered during ventricular fibrillation.
  
  
  RESULTS
  : The myocardial metabolism reflected by the concentration of lactate, or myocardial tissue PCO2 and PO2, is dramatically reduced during cardiac arrest and cardiopulmonary resuscitation. These are associated with less severe postresuscitation myocardial dysfunction and longer duration of postresuscitation survival.
  
  
  CONCLUSIONS
  delta-Opioid-induced pharmacologic myocardial hibernation is an option to minimize the myocardial ischemia and reperfusion injury during cardiac arrest and cardiopulmonary resuscitation.
authors.affiliation: Weil Institute of Critical Care Medicine, Rancho Mirage, California, USA.
authors.forename: Xiangshao
authors.initials: X
authors.lastname: Fang
authors.forename: Wanchun
authors.initials: W
authors.lastname: Tang
authors.forename: Shijie
authors.initials: S
authors.lastname: Sun
authors.forename: Max Harry
authors.initials: MH
authors.lastname: Weil
mesh_terms: D000818:Animals; D016887:Cardiopulmonary Resuscitation; D006323:Heart Arrest / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy*; D006605:Hibernation; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D017682:Myocardial Stunning / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism*; D051381:Rats; D017465:Receptors, Opioid, delta / Q000819:agonists*; D013552:Swine; D014693:Ventricular Fibrillation / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy
chemical_list: D017465:Receptors, Opioid, delta