Acetylcholine but not sodium nitroprusside exerts vasodilation in pulmonary hypertension secondary to chronic congestive heart failure

Citation
R. Wensel et al., Acetylcholine but not sodium nitroprusside exerts vasodilation in pulmonary hypertension secondary to chronic congestive heart failure, J HEART LUN, 18(9), 1999, pp. 877-883
Citations number
30
Categorie Soggetti
Cardiovascular & Respiratory Systems
Journal title
JOURNAL OF HEART AND LUNG TRANSPLANTATION
ISSN journal
10532498 → ACNP
Volume
18
Issue
9
Year of publication
1999
Pages
877 - 883
Database
ISI
SICI code
1053-2498(199909)18:9<877:ABNSNE>2.0.ZU;2-D
Abstract
Background: Reduced endothelium-dependent vasodilation contributes to the d evelopment of pulmonary hypertension in chronic congestive heart failure (C HF). We investigated pulmonary endothelium-dependent and independent vasodi lation in patients with CHF. Methods: We studied 42 patients with CHF (age 55 +/- 10, NYHA Classes II-II I, left ventricular ejection fraction 27 +/- 10%, mean PAP 29 +/- 12 mmHg). The endothelial vasodilator capacity of pulmonary resistance vessels was a ssessed by the infusion of acetylcholine into a pulmonary artery branch whi le measuring the blood flow velocity with a Doppler flow wire. For comparis on endothelium-independent vasodilation was measured with the response to s odium nitroprusside. The conductance vessel diameter (4.4 +/- 0.2 mm) was d etermined by intravascular ultrasound. Acetylcholine was administered at co ncentrations of 10(-6) to 10(-4) mol/l, sodium nitroprusside was administer ed at concentrations of 0.125 and 0.25 mu g/kg per min. The effects on cond uctance vessel diameter were investigated in 12 patients by the measurement of diameter and flow velocity following the administration of acetylcholin e and sodium nitroprusside. Results: Acetylcholine markedly increased blood flow velocity (+39 +/- 7% a t 10(-4) mol/l; p < .05). This correlated with the baseline PAP (r = 0.58; p < .05) and pulmonary vascular resistance (r = 0.58; p < .05). Sodium nitr oprusside caused a small increase in the flow velocity (5 +/- 2% at 0.125, 12 +/- 4% at 0.25 mu g/kg per minute; p < .05) that was accompanied by syst emic vasodilation. The conductance vessel diameter was unchanged after acet ylcholine was administered and was only marginally decreased after the admi nistration of sodium nitroprusside. Conclusions: In CHF acetylcholine reveals preserved receptor-mediated endot helial vasodilation, that is positively correlated to pulmonary hypertensio n, and cannot be reproduced by sodium nitroprusside.