INHALED NITRIC-OXIDE PARTIALLY REVERSES HYPOXIC PULMONARY VASOCONSTRICTION IN THE DOG

Nitric oxide (NO) inhaled during a hypoxia-induced increase in pulmona ry vasomotor tone decreases pulmonary arterial pressure (Ppa). We cond ucted this study to better characterize the hemodynamic effects induce d by NO inhalation during hypoxic pulmonary vasoconstriction in 11 ane sthetized ventilated dogs. Arterial and venous systemic and pulmonary pressures and aortic flow probe-derived cardiac output were recorded, and nitrosylhemoglobin (NO-Hb) and methemoglobin (MetHb) were measured . The effects of 5 min of NO inhalation at 0, 17, 28, 47, and 0 ppm du ring hyperoxia (inspiratory fraction of O-2 = 0.5) and hypoxia (inspir atory fraction of O-2 = 0.16) were observed. NO inhalation has no meas urable effects during hyperoxia. Hypoxia induced an increase in Ppa th at reached plateau levels after 5 min. Exposure to 28 and 47 ppm NO in duced an immediate (<30 s) decrease in Ppa and calculated pulmonary va scular resistance (P < 0.05 each) but did not return either to baselin e hyperoxic values. Increasing the concentration of NO to 74 and 145 p pm in two dogs during hypoxia did not induce any further decreases in Ppa. Reversing hypoxia while NO remained at 47 ppm further decreased P pa and pulmonary vascular resistance to baseline values. NO inhalation did not induce decreases in systemic arterial pressure. MetHb remaine d low, and NO-Hb was unmeasurable. We concluded that NO inhalation onl y partially reversed hypoxia-induced increases in pulmonary vasomotor tone in this canine model. These effects are immediate and selective t o the pulmonary circulation.