title: [Inhibition of pulmonary vasoconstriction by inhaled nitric oxide].
abstract: We examined effects of inhaled NO gas on pulmonary vasoconstriction induced with hypoxic gas or PGF2 alpha utilizing the isolated perfused rabbit lung. While NO 180 ppm did not change the basal pulmonary artery pressure, the pressure response to hypoxia or PGF2 alpha was completely inhibited by pretreatment with NO inhalation. Inhaled NO during maximal pressor response also depressed the elevated pressure to the basal level. These findings suggest that NO inhaled to the alveoli diffuses directly into the pulmonary vascular smooth muscle and then causes nonspecific vasodilation, and its effect is more potent than that of constitutive type of EDRF/NO.
authors.affiliation: Department of Anesthesiology, Faculty of Medicine, Tottori University, Yonago.
authors.forename: Y
authors.initials: Y
authors.lastname: Ohshima
authors.forename: Y
authors.initials: Y
authors.lastname: Ishibe
authors.forename: N
authors.initials: N
authors.lastname: Okazaki
authors.forename: T
authors.initials: T
authors.lastname: Sato
mesh_terms: D000280:Administration, Inhalation; D000818:Animals; D004058:Diffusion; D015237:Dinoprost / Q000037:antagonists & inhibitors; D005260:Female; D000860:Hypoxia; D066298:In Vitro Techniques; D009131:Muscle, Smooth, Vascular / Q000378:metabolism; D009609:Nitrous Oxide / Q000493:pharmacokinetics / Q000494:pharmacology*; D011651:Pulmonary Artery / Q000187:drug effects*; D011817:Rabbits; D014661:Vasoconstriction / Q000187:drug effects*
chemical_list: D015237:Dinoprost; D009609:Nitrous Oxide