THE INFLUENCE OF BASAL NITRIC-OXIDE ACTIVITY ON PULMONARY VASCULAR-RESISTANCE IN PATIENTS WITH CONGESTIVE-HEART-FAILURE

Increased pulmonary resistance may reduce survival and treatment optio ns in patients with congestive heart failure. Nitric oxide (NO) is a d eterminant of normal pulmonary resistance vessel tone. We tested the h ypothesis' that loss of NO function contributes to increased pulmonary vascular resistance index (PVRI) in congestive heart failure. Pulmona ry arterial resistance vessel function was studied in 25 conscious adu lts, Three groups were studied: 8 controls, 9 patients with congestive heart failure and normal PVRI, and 8 patients with congestive heart f ailure and raised PVRI. Segmental arterial flow was determined with a Doppler wire and quantitative angiography. N-G-monomethyl-L-arginine ( L-NMMA) was used to inhibit NO, whereas phenylephrine was used as an e ndothelium-independent control. The response to inhibition of NO with L-NMMA was less in patients with congestive heart failure and elevated PVRI than in patients with congestive heart failure and normal PVRI ( p < 0.05). The difference in response between the congestive heart fai lure groups was specific to NO-dependent regulation because the respon se to the endothelium-independent constrictor phenylephrine was not di fferent (p = 0.92). There was no difference in response to L-NMMA betw een controls and patients with congestive heart failure and normal PVR I. The response to L-NMMA correlated to PVRI. In adults with congestiv e heart failure, NO appears to play an important role in maintaining n ormal pulmonary resistance. (C) 1998 by Excerpta Medica, Inc.