Habib F, Dutka D, Crossman D, Oakley C M, Cleland J G
Department of Medicine (Cardiology), Royal Postgraduate Medical School, Hammersmith Hospital, London, UK.
Lancet. 1994 Aug 6;344(8919):371-3. doi: 10.1016/s0140-6736(94)91402-8.
Endothelial dysfunction in heart failure could impair nitric oxide production and lead to increased vascular resistance. If endogenous production of nitric oxide is reduced, NG-monomethyl-L-arginine (L-NMMA), an inhibitor of such production, should have a diminished vasoconstrictor effect. We administered L-NMMA to 12 patients being investigated for heart failure. L-NMMA increased median pulmonary and systemic vascular resistances by 61 (range -3 to 240) and 430 (63 to 1609) dynes s cm-5, respectively (p < 0.03 and p < 0.005). Arterial pressures also increased. Median cardiac output fell by 0.6 (0 to -2.3) L per min (p < 0.005). These data suggest that vascular nitric oxide may be another example of a failed counter-regulatory vasodilator system in heart failure.
