title: [Absence of the effect of nitric oxide on pulmonary and systemic hypertension induced by sino-aortic denervation].
abstract: Inhaled nitric oxide, a selective pulmonary vasodilator, reverses hypoxic pulmonary vasoconstriction and is an effective treatment in some cases of human pulmonary hypertension. Localization of nitric oxide synthase had indicated a neural role for nitric oxide. Thus, we studied the interactions between inhaled nitric oxide and systemic and pulmonary vascular reactivity in acute neurogenic hypertension. In 6 male beagle dogs (mean weight: 15 +/- 1 kg), anesthetized by chloralose (8 cg/kg) and in spontaneous ventilation, the hemodynamic effects on systemic and pulmonary circulation of inhaled nitric oxide (12 ppm) were studied before and after acute sino-aortic denervation. The hemodynamic effects of intravenous propranolol (300 micrograms/kg) were studied after denervation. Mean arterial pressure (MAP), pulmonary capillary pressure (PCP), mean arterial pulmonary pressure (MAPP), cardiac input (CI) and oxygen venous saturation (SvO2) were measured. [table: see text] Sino-aortic denervation causes an acute and transitory pulmonary hypertension due to a double mechanism: a post-capillary hypertension (increase PCP) secondary to an increase left ventricular post-charge by systemic hypertension and a precapillary hypertension. In fact, vascular pulmonary resistances increase from 1.8 +/- 0.1 to 3.4 +/- 0.8 uW after denervation (p < 0.05). Change in pulmonary vascular reactivity induced by catecholamines is probably involved. Propranolol but not inhaled nitric oxide reverse pulmonary hypertension due to sino-aortic denervation.
authors.affiliation: Service de cardiologie et de chirurgie cardiovasculaire, Hôpital Rangueil, Toulouse.
authors.forename: M
authors.initials: M
authors.lastname: Galinier
authors.forename: P
authors.initials: P
authors.lastname: Rougé
authors.forename: J P
authors.initials: JP
authors.lastname: Albenque
authors.forename: B
authors.initials: B
authors.lastname: Assoun
authors.forename: P
authors.initials: P
authors.lastname: Massabuau
authors.forename: J M
authors.initials: JM
authors.lastname: Fauvel
authors.forename: J P
authors.initials: JP
authors.lastname: Bounhoure
authors.forename: J L
authors.initials: JL
authors.lastname: Montastruc
authors.forename: P
authors.initials: P
authors.lastname: Montastruc
mesh_terms: D000280:Administration, Inhalation; D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology / Q000627:therapeutic use; D002346:Carotid Sinus / Q000503:physiopathology; D003714:Denervation; D004285:Dogs; D006439:Hemodynamics; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000503:physiopathology*; D008297:Male; D009569:Nitric Oxide / Q000502:physiology* / Q000627:therapeutic use; D011433:Propranolol / Q000494:pharmacology / Q000627:therapeutic use; D014628:Vagotomy
chemical_list: D000959:Antihypertensive Agents; D009569:Nitric Oxide; D011433:Propranolol
vernacular_title: Absence d'effet du monoxyde d'azote sur l'hypertension artérielle pulmonaire et systémique induite par la défrénation sino-aortique.