Am. J. Respir. Crit. Care Med., Vol 151, No. 2, Feb 1995, 384-389.
Inhaled nitric oxide as a screening vasodilator agent in primary pulmonary hypertension. A dose-response study and comparison with prostacyclin
O Sitbon, F Brenot, A Denjean, A Bergeron, F Parent, R Azarian, P Herve, B Raffestin and G Simonneau
Service de Pneumologie et Reanimation, Hopital Antoine Beclere, Clamart, France.
To investigate the capacity of the pulmonary vascular bed to acutely
vasodilate, we examined in 35 consecutive patients with primary pulmonary
hypertension (PPH), the hemodynamic effects of incremental inhalation
periods of an air-NO mixture at different concentrations (10, 20, and 40
ppm), and compared them with those of an acute infusion of prostacyclin
(PGI2). An individual pulmonary vasodilator response was defined by a fall
in total pulmonary resistance (TPR) > or = 30% relative to mean TPR
baseline value. Thirteen patients were responders and 22 were nonresponders
to both drugs, and they did not significantly differ in overall baseline
characteristics except for mean right atrial pressure (p < 0.03). In
responders, both drugs produced similar individual vasodilator response.
Changes in mean pulmonary arterial pressure and TPR observed during NO and
PGI2 were closely correlated (r2 = 0.9, p < 0.001, and r2 = 0.7, p <
0.01, respectively). The vasodilator response to NO was not
concentration-related with a maximal effect obtained at 10 ppm. Combination
of both drugs did not lead to any additive vasodilator response. Unlike
PGI2, NO did not induce any systemic effect, no adverse reaction, but a
moderate increase in methemoglobin. Inhaled NO at low dose (10 ppm) appears
to be an effective, safe, and reliable substitute for PGI2 in screening for
acute pulmonary vasodilator responsiveness during therapeutic assessment of
patients with PPH.
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Surgery with cardiopulmonary bypass and pulmonary inflammatory responses
Perfusion,
May 1, 1996;
11(3):
213 - 219.
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