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Am J Physiol Heart Circ Physiol 277: H2442-H2450, 1999;
0363-6135/99 $5.00
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Vol. 277, Issue 6, H2442-H2450, December 1999

SPECIAL TOPIC
Met5-enkephalin protects isolated adult rabbit cardiomyocytes via delta -opioid receptors

Yasushi Takasaki1, Roger A. Wolff2, Grace L. Chien1,2, and Donna M. van Winkle1,2

1 Department of Anesthesiology, Oregon Health Sciences University, Portland 97201; and 2 Research and Anesthesiology Services, Veterans Affairs Medical Center, Portland, Oregon 97201

In rats and rabbits, endogenous opioid peptides participate in ischemic preconditioning. However, it is not known which endogenous opioid(s) can trigger cardioprotection. We examined preconditioning-induced and opioid-induced limitation of cell death in isolated, calcium-tolerant, adult rabbit cardiomyocytes. Cells were subjected to simulated ischemia by pelleting and normothermic hypoxic incubation. Preconditioning was elicited with 15 min of simulated ischemia followed by 15 min of resuspension and reoxygenation. All cells underwent 180 min of simulated ischemia. Cell death was assessed by trypan blue permeability. Morphine protected cells, as did preconditioning; naloxone blocked the preconditioning-induced protection. Exogenous Met5-enkephalin (ME) induced protection, but exogenous beta -endorphin did not. ME-induced protection was blocked by the delta -selective antagonist naltrindole. Additionally, two other proenkephalin products, Leu5-enkephalin and Met5-enkephalin-Arg-Phe, provided protection equipotent to ME. These data suggest that one or more proenkephalin products interact with delta -opioid receptors to endogenously trigger opioid-mediated protection.

heart; opioid peptides; hypoxia; cell viability


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