Relation between impairment in nitric oxide pathway and clinical status in patients with congestive heart failure

A dissociation between basal and stimulated release of nitric oxide (NO) has been found in the peripheral vasculature of patients with congestive heart failure. To explore basal and stimulated NO-mediated vasodilation in patients with heart failure of varying severity, three groups of subjects were studied: group 1, eight normal subjects; group 2, six patients with moderate heart failure; and group 3, eight patients with severe heart failure. Forearm blood flow (FBF) was measured by plethysmography in response to local brachial infusion of acetylcholine, N(G)-monomethyl-L-arginine (L-NMMA), sodium nitroprusside (SNP), and noradrenaline (NA). The vasodilating response to acetylcholine was markedly impaired in patients with severe heart failure compared with the other groups, with FBF increasing by 59 +/- 19% in group 3 vs. 220 +/- 64% in group 2 (p < 0.05) and 586 +/- 168% in group 1 (p < 0.01) at 80 microg/min acetylcholine. As compared with controls, vasodilation to SNP was impaired in group 3 but unchanged in group 2. NA caused similar vasoconstrictor response in the three groups, whereas vasoconstriction to L-NMMA was less marked in group 3. These results show that vasodilator responses to both acetylcholine and SNP are impaired in patients with heart failure and that this impairment is related to the clinical severity of heart failure.