Increased nitric oxide production in heart failure

D. S. Winlaw, A. M. Keogh, C. G. Schyvens, P. M. Spratt, P. S. Macdonald*, G. A. Smythe

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

249 Scopus citations

Abstract

The role of nitric oxide in heart failure is unknown. The high-capacity inducible isoform of nitric oxide synthase is present in the myocardium of patients with idiopathic dilated cardiomyopathy. Plasma nitrate, the stable end-product of nitric oxide production, was significantly increased in patients with heart failure compared with normal controls (means 51·3 and 24·6 μmol/L). Vasodilation caused by increased nitric oxide may compensate for the vasoconstrictor effect of neurohumoral adaptions to heart failure. Alternatively, excess production may be detrimental to the heart by a direct negative inotropic effect.

Original languageEnglish (US)
Pages (from-to)373-374
Number of pages2
JournalThe Lancet
Volume344
Issue number8919
DOIs
StatePublished - Aug 6 1994

ASJC Scopus subject areas

  • General Medicine

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