M. Sakane et al., INHALED NITRIC-OXIDE IN PATIENTS WITH PULMONARY-HYPERTENSION DUE TO VALVULAR HEART-DISEASE AND CHRONIC LUNG-DISEASE, Japanese Circulation Journal, 62(12), 1998, pp. 877-882
The objective of this study was to investigate the effects of inhaled
nitric oxide (NO) on chronic pulmonary hypertension (PH). Thirty patie
nts with valvular heart diseases (n=8, group A), chronic lung diseases
(n=16, group B), primary PH or PH due to collagen disease (n=6, group
C) were studied. NO was delivered for 20min at concentration of 5, 10
, and 20ppm in spontaneous respiration. After inhalation, percentages
of systolic pulmonary artery pressure (%SPAP) levels in group A were s
ignificantly decreased compared with those for preinhalation by 12%, 1
4%, and 14% at 5, 10 and 20ppm, respectively (p<0.05). In group B, %SP
AP also significantly decreased by 7, 10, and 14% at 5, 10, and 20ppm,
respectively (p<0.05). However, inhaled NO did not significantly affe
ct %SPAP in group C (p=0.4). There was no significant difference in ga
s exchange in any of the groups. However, 4 out of 8 patients in group
A and 10 out of 16 patients in group B showed decreased partial press
ure of arterial oxygen in response to inhaled NO. This study demonstra
ted that inhaled NO is a selective pulmonary vasodilator in decreasing
pulmonary artery pressure (PAP); however, the reaction was different
in line with the background disease cause of PH. NO inhalation was mos
t effective on patients with moderate PAP. Furthermore, higher concent
rations of NO would be risky in some patients with chronic PH.