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Ann Thorac Surg 2001;72:1576-1582
© 2001 The Society of Thoracic Surgeons
a Department of Anesthesiology, University of Minnesota, Minneapolis, Minnesota, USA
b Department of Physiology, University of Minnesota, Minneapolis, Minnesota, USA
c Biomedical Engineering Institute, University of Minnesota, Minneapolis, Minnesota, USA
d Department of Pathology, University of Kentucky, Lexington, Kentucky, USA
Accepted for publication June 28, 2001.
* Address reprint requests to Dr Iaizzo, Department of Anesthesiology, University of Minnesota, 420 Delaware St SE, MMC 294 UMHC, Minneapolis, MN 55455, USA
e-mail: iaizz001{at}tc.umn.edu
Background. Opioid receptor agonists are involved in ischemic preconditioning and natural hibernation. The aim of this study was to determine whether pretreatment with D-Ala2-Leu5-enkephalin or morphine confers cardioprotection in large mammalian hearts. We assessed myocardial functional recovery and global energy metabolism after ischemic cold storage.
Methods. After pretreatment with D-Ala2-Leu5-enkephalin, morphine sulfate, or saline (n = 6 each), swine hearts were excised and stored for 75 minutes at 4°C, then reperfused in a four-chamber isolated working heart apparatus. Serial myocardial biopsies were performed to assess cellular energy metabolism.
Results. Improved systolic (cardiac output, contractility) and diastolic (tau) left ventricular functions were observed in hearts pretreated with D-Ala2-Leu5-enkephalin or morphine. These benefits were not correlated with changes in high-energy phosphate levels. Cardiac enzyme leakage (creatine kinase, troponin-I) was similar among treated and control groups. Lactate efflux increased significantly in controls, but not in opioid-pretreated hearts (p < 0.01) at 75 minutes of reperfusion.
Conclusions. D-Ala2-Leu5-enkephalin and morphine pretreatments improve postischemic function after cold storage of swine hearts. Postischemic lactate reduction, but not high-energy phosphate levels, may account for the observed cardioprotective effects.
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