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
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.