Circulation, Vol 88, 2128-2138, Copyright © 1993 by American Heart Association
DL Wessel, I Adatia, TM Giglia, JE Thompson and TJ Kulik
BACKGROUND. Increased pulmonary vascular resistance is common in congenital
heart disease and is exacerbated by cardiopulmonary bypass (CPB). We
investigated whether CPB is responsible for pulmonary endothelial
dysfunction and contributes to postoperative pulmonary hypertension.
METHODS AND RESULTS. We infused the endothelium-dependent vasodilator
acetylcholine (ACH) into the pulmonary circulation of pulmonary
hypertensive children with congenital heart disease either before (n = 12)
or after (n = 22) surgical repair on CPB. The dose response to ACH (10(-9)
to 10(-6) M) was recorded for all hemodynamic variables. Nine additional
postoperative patients were studied with ACH followed by inhalation of 80
ppm nitric oxide, an endothelium- independent smooth muscle relaxant.
Plasma levels of cyclic GMP (cGMP) were measured before and after ACH and
nitric oxide administration. Pulmonary vasodilation with 10(-6) M ACH was
seen in all preoperative patients but was markedly attenuated in
postoperative patients. Baseline pulmonary vascular resistance (5.6 +/- 1.0
U x m2) fell 46 +/- 5% in preoperative patients but declined only 11 +/- 4%
from baseline (5.8 +/- 0.9 U x m2) in postoperative patients (P < .002).
However, inhalation of 80 ppm nitric oxide after ACH infusion in
postoperative patients lowered pulmonary vascular resistance by 33 +/- 4%
(P < .0002 compared with postoperative ACH response) with minimal
effects on the systemic circulation. This finding suggests that the
capacity for smooth muscle relaxation and pulmonary vasodilation was
present in postoperative patients but could not be induced by ACH. Plasma
levels of cGMP in postoperative patients were unchanged after acetylcholine
infusion but rose more than threefold during pulmonary vasodilation with
nitric oxide (P < .0001). This finding is consistent with the purported
role of cGMP as the second messenger effecting smooth muscle relaxation in
this process. CONCLUSIONS. CPB may be responsible for postoperative
dysfunction of the pulmonary endothelial cell and may contribute to
postoperative pulmonary hypertension in children. Inhaled nitric oxide is a
potent pulmonary vasodilator after CPB with minimal systemic circulatory
effects. It may have important diagnostic and therapeutic applications in
patients with congenital heart disease.
ARTICLES
Use of inhaled nitric oxide and acetylcholine in the evaluation of pulmonary hypertension and endothelial function after cardiopulmonary bypass
Department of Cardiology, Children's Hospital, Boston, MA 02115.
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