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Published on: April 19, 2011
Opioid preconditioning: myocardial function and energy metabolism
D C Sigg1, J A Coles, W J Gallagher
1Department of Anesthesiology, University of Minnesota, Minneapolis, 55455, USA.
Opioid receptor agonists like D-Ala2-Leu5-enkephalin and morphine protect large mammalian hearts from ischemic injury. Pretreatment improves heart function after cold storage by reducing lactate efflux, not by altering energy phosphate levels.
Area of Science:
- Cardiology
- Pharmacology
- Physiology
Background:
- Opioid receptor agonists are implicated in ischemic preconditioning and natural hibernation.
- This study investigated the cardioprotective potential of D-Ala2-Leu5-enkephalin and morphine in large mammalian hearts.
- Myocardial functional recovery and energy metabolism following ischemic cold storage were assessed.
Purpose of the Study:
- To determine if D-Ala2-Leu5-enkephalin or morphine pretreatment confers cardioprotection in large mammalian hearts.
- To evaluate the effects of these opioid agonists on myocardial functional recovery and energy metabolism after ischemic cold storage.
Main Methods:
- Swine hearts were pretreated with D-Ala2-Leu5-enkephalin, morphine sulfate, or saline.
- Hearts underwent 75 minutes of cold storage at 4°C, followed by reperfusion in an isolated working heart apparatus.
- Myocardial biopsies were taken serially to assess cellular energy metabolism.
Main Results:
- Pretreatment with D-Ala2-Leu5-enkephalin or morphine significantly improved systolic and diastolic left ventricular functions.
- No correlation was found between functional improvements and changes in high-energy phosphate levels.
- Opioid pretreatment prevented the significant increase in lactate efflux observed in control hearts during reperfusion.
Conclusions:
- D-Ala2-Leu5-enkephalin and morphine pretreatments enhance postischemic cardiac function in swine hearts after cold storage.
- Reduced postischemic lactate efflux, rather than altered high-energy phosphate levels, may mediate the observed cardioprotective effects.
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