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

doi:10.1016/S0140-6736(94)91403-6

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

Surgery

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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 language	English (US)
Pages (from-to)	373-374
Number of pages	2
Journal	The Lancet
Volume	344
Issue number	8919
DOIs	https://doi.org/10.1016/S0140-6736(94)91403-6
State	Published - Aug 6 1994

ASJC Scopus subject areas

General Medicine

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title = "Increased nitric oxide production in heart failure",

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.",

author = "Winlaw, {D. S.} and Keogh, {A. M.} and Schyvens, {C. G.} and Spratt, {P. M.} and Macdonald, {P. S.} and Smythe, {G. A.}",

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AU - Winlaw, D. S.

AU - Keogh, A. M.

AU - Schyvens, C. G.

AU - Spratt, P. M.

AU - Macdonald, P. S.

AU - Smythe, G. A.

PY - 1994/8/6

Y1 - 1994/8/6

N2 - 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.

AB - 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.

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Increased nitric oxide production in heart failure

Abstract

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