-
- D S Winlaw, G A Smythe, A M Keogh, C G Schyvens, P M Spratt, and P S Macdonald.
- Department of Cardiopulmonary Transplantation, Victor Chang Cardiac Research Institute, St Vincent's Hospital, Sydney, Australia.
- Lancet. 1994 Aug 6; 344 (8919): 373-4.
AbstractThe 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 mumol/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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