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En Face Detection of Nitric Oxide and Superoxide in Endothelial Layer of Intact Arteries
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Nitric oxide modulates myocardial oxygen consumption in the failing heart

YingJie Chen1, Jay H Traverse, Ruisheng Du

  • 1Department of Medicine, Division of Cardiology, University of Minnesota Medical School, Minneapolis 55455, USA.

Circulation
|July 10, 2002
PubMed
Abstract

Insights

In congestive heart failure, inhibiting inducible nitric oxide synthase (iNOS) increases myocardial oxygen consumption (MVO2). This suggests iNOS plays a key role in regulating MVO2 in failing hearts.

Area of Science:

  • Cardiovascular Physiology
  • Nitric Oxide Biology

Background:

  • Endogenous nitric oxide (NO) normally inhibits myocardial oxygen consumption (MVO2).
  • Nonselective nitric oxide synthase (NOS) inhibition increases MVO2 in healthy hearts.
  • Endothelial NOS is impaired in congestive heart failure (CHF), but inducible NOS (iNOS) may be present.

Purpose of the Study:

  • To test if NOS inhibition increases MVO2 in the failing heart.
  • To investigate the role of iNOS in MVO2 regulation in CHF.

Main Methods:

  • Congestive heart failure (CHF) induced in dogs via rapid ventricular pacing.
  • Selective iNOS inhibition using S-methylisothiourea.
  • Measurement of MVO2, coronary blood flow, left ventricular pressure, and dP/dt at rest and during exercise.

Main Results:

  • CHF dogs showed reduced resting coronary blood flow and MVO2, with blunted exercise response.
  • Selective iNOS inhibition increased MVO2 at rest and during exercise in CHF dogs.
  • iNOS inhibition had no effect on MVO2 in normal dogs, unlike nonselective NOS inhibition.

Conclusions:

  • Endogenous NO modulates MVO2 in failing hearts.
  • iNOS contributes to NO production in CHF myocardium.
  • The source of NO modulating MVO2 differs between normal and failing hearts.

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