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Kappa opioid receptor mediates the cardioprotection of postconditioning in the isolated rat heart subjected to ischemia and reperfusion
Author(s) -
Wang Jue,
Gao Qin,
Lu Yuan,
Xia Qiang
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a742-c
Subject(s) - cardioprotection , ischemia , (+) naloxone , opioid receptor , agonist , pharmacology , κ opioid receptor , reperfusion injury , antagonist , medicine , opioid , lactate dehydrogenase , chemistry , anesthesia , receptor , biochemistry , enzyme
The aim of this study was to investigate whether the opioid receptors contribute to cardioprotection elicited by ischemic postconditioning. Male Sprague‐Dawley rat hearts were subjected to 30 min of global ischemia followed by 120 min of reperfusion. Formazan, which is proportional to myocardial viability, was measured at 490 nm spectrophotometrically, and the level of lactate dehydrogenase (LDH) in the coronary effluent was measured. In the Langendorff perfused rat heart, postconditioning (6 cycles of 10 s reperfusion/10 s global ischemia starting at the beginning of reperfusion) increased formazan content, reduced LDH release, improved hemodynamic parameters during reperfusion. Pretreatment with naloxone (3mg/kg, i.v.), a universal opioid receptor antagonist, attenuated the effect of postconditioning. Perfusion with the selective kappa opioid receptor antagonist nor‐binaltorphimine (30 nmol/L, perfused for 15 min after ischemia) also attenuated the effect of postconditioning. The specific mitochondrial ATP sensitive K + channel (mitoK ATP ) antagonist 5‐hydroxydecanoate (100 micromol/L, perfused for 10 min after ischemia) abolished the effect of postconditioning and the protective effect of pretreatment with kappa opioid receptor agonist U50,488H prior the ischemia. The results indicate that in the isolated rat heart, ischemic postconditioning protects myocardium against ischemia/reperfusion injury via activating kappa opioid receptor and mitoK ATP may be the downstream of kappa opioid receptor activation. (Supported by ZJSTB grant No.2005C30026)