Y. Katayama et al., EFFECTS OF INHALED NITRIC-OXIDE IN RATS WITH CHEMICALLY-INDUCED PULMONARY-HYPERTENSION, Respiration physiology, 97(3), 1994, pp. 301-307
To determine the model animal with pulmonary hypertension in which nit
ric oxide (NO) inhalation reduces pulmonary arterial pressure (PAP), w
e examined the inhalation of 20-100 ppm NO gas on normal rats and rats
with monocrotaline induced pulmonary hypertension. In the control gro
up, mean PAP showed no change after spontaneous breathing of NO at the
concentration of 20 to 100 ppm for 5 min. On the contrary, in both th
e severe (mean PAP>40 mmHg) and moderate (mean PAP<40 mmHg) pulmonary
hypertensive groups, NO inhalation produced a prompt reduction of the
mean PAP which had been elevated by monocrotaline. 20 ppm NO inhalatio
n reduced mean PAP from 64.4 +/- 3.7 mmHg to 56.2 +/- 4.4 mmHg (mean /- SEM, P<0.01) in the severe pulmonary hypertensive group, from 31.0
+/- 2.0 mmHg to 24.2 +/- 0.9 mmHg in the moderate pulmonary hypertensi
ve group (mean +/- SEM, P<0.05). The onset of the reduction of mean PA
P occurred within 30 sec after the start of NO inhalation and maximum
reduction occurred within 4 min. 20 ppm NO inhalation significantly re
duced mean PAP, and mean PAP was reduced dose-dependently at the conce
ntration of 20 to 60 ppm and reaction to NO was almost constant at the
concentrations of over 60 ppm.