Winlaw D S, Smythe G A, Keogh A M, Schyvens C G, Spratt P M, Macdonald P S
Department of Cardiopulmonary Transplantation, Victor Chang Cardiac Research Institute, St Vincent's Hospital, Sydney, Australia.
Lancet. 1994 Aug 6;344(8919):373-4. doi: 10.1016/s0140-6736(94)91403-6.
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 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.
