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Intermittent hypoxia conditioning restricts iNOS and eNOS expression in rat myocardium: a mechanism for protection from ischemia and reperfusion injury (710.4)
Author(s) -
Manukhina Eugenia,
Goryacheva Anna,
Belkina Ludmila,
Terekhina Olga,
Mallet Robert,
Downey H
Publication year - 2014
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.28.1_supplement.710.4
Subject(s) - enos , nitrotyrosine , nitric oxide , nitric oxide synthase , hypoxia (environmental) , immunohistochemistry , medicine , reperfusion injury , ligation , ischemia , endocrinology , chemistry , oxygen , organic chemistry
Recently we demonstrated that intermittent, normobaric hypoxia conditioning (IHC) prevented injuries of myocardium and coronary blood vessels induced by myocardial ischemia and reperfusion (IR). This cardio‐ and vasoprotection of was associated with alleviation of nitric oxide overproduction. The aim of this study was to identify specific NO synthase(s) responsible for the IR‐induced NO overproduction and to determine the effect of IHC on these NO synthases. IHC of rats was performed in a normobaric chamber (5‐8 cycles/d for 20 d, FIO 2 9.5 ‐ 10% for 5 ‐ 10 min/cycle, with intervening 4‐min normoxia). IR was produced by ligation of the left anterior descending coronary artery for 30 min followed by 60‐min reperfusion. The protein nitration marker, nitrotyrosine (3‐NT) and neuronal (nNOS), inducible (iNOS), and endothelial (eNOS) nitric oxide synthases were measured by immunoblot. IR induced appreciable 3‐NT accumulation in the left ventriclular free wall, increasing the 3‐NT content by 42% (p<0.01), but not in septum. In IHC rats, 3‐NT after IR was similar to that of control rats without IR. IHC decreased iNOS by 71% (p<0.05) and eNOS by 41% (p<0.05) in the left ventricular myocardium; the myocardial content of nNOS remained unchanged. Therefore, IHC prevents IR‐induced NO overproduction in myocardium by restricting myocardial expression of iNOS and eNOS. Grant Funding Source : Supported by the Russian Foundation for Basic Research grant 10‐04‐00980