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Title: Inhaled nitric oxide partially reverses hypoxic pulmonary vasoconstriction in the dog

Journal Article · · Journal of Applied Physiology (1985); (United States)
OSTI ID:7060554

Nitric oxide (NO) inhaled during a hypoxia-induced increase in pulmonary vasomotor tone decreases pulmonary arterial pressure (Ppa). The authors conducted this study to better characterize the hemodynamic effects induced by NO inhalation during hypoxic pulmonary vasoconstriction in 11 anesthetized ventilated dogs. Arterial and venous systematic 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 during hyperoxia (inspiratory fracture of O[sub 2] = 0.5) and hypoxia (inspiratory fraction of O[sub 2] = 0.16) were observed. NO inhalation has no measurable effects during hyperoxia. Hypoxia induced an increase in Ppa that reached plateau levels after 5 min. Exposure to 28 and 47 ppm NO induced an immediate (<30 s) decrease in Ppa and calculated pulmonary vascular resistance (P < 0.05 each) but did not return either to baseline hyperoxic values. Increasing the concentration of NO to 74 and 145 ppm further decreased Ppa and pulmonary vascular resistance to baseline values. NO inhalation did not induce decreases in systematic arterial pressure. MetHb remained low, and NO-Hb was ummeasurable. The authors concluded that NO inhalation only partially reversed hypoxia-induced increases in pulmonary vasomotor tone in this canine model. These effects are immediate and selective to the pulmonary circulation. 26 refs., 3 figs., 2 tabs.

OSTI ID:
7060554
Journal Information:
Journal of Applied Physiology (1985); (United States), Vol. 76:3; ISSN 8750-7587
Country of Publication:
United States
Language:
English