E. Troncy et al., COMPARISON OF THE EFFECT OF INHALED NITRIC-OXIDE AND INTRAVENOUS NITROGLYCERINE ON HYPOXIA-INDUCED PULMONARY-HYPERTENSION IN PIGS, European journal of anaesthesiology, 13(5), 1996, pp. 521-529
Pulmonary hypertension is usually treated with intravenous (i.v.) vaso
dilators, but their use is limited by systemic effects. In the current
study, we compared the effects of inhaled nitric oxide and intravenou
s nitroglycerine on pulmonary and systemic haemodynamic responses as w
ell as on gas exchange measurements in anaesthetized pigs whose pulmon
ary pressure was increased by hypoxia (FiO(2)=15%). Both treatments re
duced pulmonary pressure to the control level. Inhaled nitric oxide di
d not affect systemic arterial pressure but intravenous nitroglycerine
decreased it from 126.2 to 108.8 mmHg (P=0.04). Unlike intravenous ni
troglycerine, inhaled nitric oxide increased arterial PaO2 from 5.3 to
5.9 kPa (P=0.02). Both treatments diminished central venous pressure
and left atrial pressure, suggesting a possible cardiac effect. Inhale
d nitric oxide was shown to be a potent pulmonary vasodilator which at
tenuated pulmonary hypertension and improved arterial oxygenation with
out important direct effects on systemic pressure in porcine hypoxia-i
nduced pulmonary hypertension.