We studied the role of the δ, µ, and к opioid receptor (OR)
subtypes in the cardioprotective effect of chronic continuous
normobaric hypoxia (CNH) in the model of acuteanoxia/
reoxygenation of isolated cardiomyocytes. Adaptation of rats to
CNH was performed by their exposure to atmosphere containing
12 % of O2 for 21 days. Anoxia/reoxygenation of cardiomyocytes
isolated from normoxic control rats caused the death of 51 % of
cells and lactate dehydrogenase (LDH) release. Adaptation of rats
to CNH resulted in the anoxia/reoxygenation-induced
cardiomyocyte death of only 38 %, and reduced the LDH release.
Pre-incubation of the cells with either the non-selective OR
blocker naloxone (300 nM/l), the δ OR antagonist TIPP(ψ)
(30 nM/l), the selective δ2 OR antagonist naltriben (1 nM/l) or the
μ OR antagonist CTAP (100 nM/l) for 25 minutes before anoxia
abolished the reduction of cell death and LDH release afforded by
CNH. The antagonist of δ1 OR BNTX (1 nM/l) or the κ OR
antagonist nor-binaltorphimine (3 nM/l) did not influence the
cytoprotective effects of CNH. Taken together, the cytoprotective
effect of CNH is associated with the activation of the δ2 and μ OR
localized on cardiomyocytes.