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Intermittent Hypoxia Conditioning (IHC) and Delta Opioid Receptor (DOR) Expression in Canine Atrium
Author(s) -
Estrada Juan,
Mallet Robert,
Downey H,
Caffrey James
Publication year - 2015
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.29.1_supplement.954.2
Subject(s) - naltrindole , immunohistochemistry , cholinergic , medicine , hypoxia (environmental) , endocrinology , stimulation , blockade , anesthesia , receptor , opioid receptor , antagonist , chemistry , organic chemistry , oxygen
Extended hypoxia exposures make hearts vulnerable to damage and reportedly suppress DOR expression in cell models resulting in cell damage. However, 20 days of limited daily IHC produced a robust resistance to ischemia reperfusion injury in canine hearts ( Exp Biol Med 2004; 229: 806‐812). DOR blockade with naltrindole during daily IHC abrogates this cardioprotection. Since DOR stimulation enhances cardioprotective cholinergic systems this study evaluated whether controlled IHC alters DOR, cholinergic and/or adrenergic systems to augment cholinergic control of the heart during ischemia reperfusion. Dogs underwent normoxic sham conditioning, IHC [5‐8 cycles of 5‐10 min hypoxia (9.5‐10% FIO 2 ) + 4 min normoxia], or IHC + daily sc naltrindole before IHC, for 20 d. On day 21, atrial tissue was biopsied for immunoblot analysis of proteins. Relative to sham values, after IHC DORs trended lower but after IHC + naltrindole were higher relative to sham (p<0.05) and IHC (p<0.01). Since DOR blockade abrogates IHC mediated protection, these data suggest that DOR stimulation during IHC down‐regulates DOR with a compensatory increase after DOR blockade. Atrial tyrosine hydroxylase was largely unchanged following IHC, while multiple markers of cholinergic function were mixed, resulting in a potential increase in cholinergic influence.