Abstract Title

INTERMITTENT HYPOXIA CONDITIONING REDUCES INOS AND ENOS EXPRESSION IN RAT MYOCARDIUM: A MECHANISM FOR PROTECTION FROM ISCHEMIA AND REPERFUSION INJURY

Presenter Name

Eugenia B. Manukhina

Abstract

During a heart attack, the heart produces excessive amounts of harmful chemicals. This study showed that prior exposure of rats to short cycles of a low oxygen atmosphere reduced production of these chemicals and lessened the damage to muscle and blood vessels of the heart. This procedure may benefit humans at risk of heart attack.

Presentation Type

Poster

Purpose (a):

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 synthases responsible for the IR-induced NO overproduction and to determine the effects of IHC on these NO synthases.

Methods (b):

This research was approved by the Animal Care and Use Committee of the Institute of General Pathology and Pathology. IHC of rats was performed in a normobaric chamber (5-8 cycles/d for 20 d, FIO2 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.

Results (c):

IR induced appreciable 3-NT accumulation in the left ventricular 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.

Conclusions (d):

IHC prevents IR-induced NO overproduction in myocardium by restricting myocardial expression of iNOS and eNOS.

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INTERMITTENT HYPOXIA CONDITIONING REDUCES INOS AND ENOS EXPRESSION IN RAT MYOCARDIUM: A MECHANISM FOR PROTECTION FROM ISCHEMIA AND REPERFUSION INJURY

During a heart attack, the heart produces excessive amounts of harmful chemicals. This study showed that prior exposure of rats to short cycles of a low oxygen atmosphere reduced production of these chemicals and lessened the damage to muscle and blood vessels of the heart. This procedure may benefit humans at risk of heart attack.