EFFECT OF INHALED NITRIC-OXIDE ON HEMODYNAMICS AND V-A/Q INEQUALITIES IN PATIENTS WITH CHRONIC OBSTRUCTIVE PULMONARY-DISEASE

被引:68
作者
MOINARD, J
MANIER, G
PILLET, O
CASTAING, Y
机构
[1] UNIV BORDEAUX 2,FAC MED VICTOR PACHON,PHYSIOL LAB,F-33076 BORDEAUX,FRANCE
[2] HOP PELLEGRIN,SERV EXPLORAT FONTIONELLE RESP,F-33076 BORDEAUX,FRANCE
[3] HOP PELLEGRIN,SERV REANIMAT MED A,F-33076 BORDEAUX,FRANCE
关键词
D O I
10.1164/ajrccm.149.6.8004302
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
Nitric oxide (NO) has been reported to be an endothelium-derived relaxing factor, and hypoxic pulmonary vasoconstriction seems to be enhanced by inhibitors of endothelially dependent vascular relaxation. We examined the circulatory effects of inhalation of 15 ppm NO in air in 14 hypoxic patients suffering from chronic obstructive pulmonary disease (COPD). Of these patients 4 breathed 100% O-2 before NO. The effects of NO inhalation on pulmonary gas exchange were also studied in 12 of these patients using the multiple inert gas elimination technique, 3 of whom breathed air, 100% O-2, and 15 ppm NO in air in succession. Under baseline conditions, both mean +/- SD pulmonary artery pressure and pulmonary vascular resistance were increased (($) over bar Ppa = 24.3 +/- 10.4 mm Hg and PVR = 3.3 +/- 1.1 mm Hg/L/min, respectively). Although the pulmonary circulatory effects were not immediate, with no detectable changes after 1 min NO inhalation, ($) over bar Ppa and PVR fell significantly (-19.1 +/- 10.5%, p < 0.02 and -29.3 +/- 15.1%, p < 0.02, respectively) after 10 min NO inhalation. Moreover, the extent of the NO-induced reduction in ($) over bar Ppa was found to depend on the level of baseline pulmonary arterial hypertension. No systemic circulatory effects were observed. The mean VA/Q ratio and the dispersion of ventilation and blood flow distributions were not altered by NO inhalation, although there was a significantly higher percentage of ventilation (7.3 +/- 7.5%, p < 0.05) in poorly and unperfused areas (VA/Q > 10). In the four subjects who breathed 100% O-2 during 20 min before NO, O-2 breathing induced a fall in both ($) over bar Ppa and cardiac output without change in PVR and with no alteration in VA/Q distributions. We conclude that inhaled NO acts as a selective pulmonary arterial vasodilator in patients with COPD. The effect has a rapid onset, even in the four patients in whom possible HPV was not reversed by 100% O-2. It seems to be associated with a slight bronchodilator effect.
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页码:1482 / 1487
页数:6
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