Inhalation of a nitric oxide synthase inhibitor to a hypoxic or collapsed lung lobe in anaesthetized pigs: effects on pulmonary blood flow distribution (original) (raw)
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Research in Veterinary Science, 1997
The effect of inhaling nitric oxide in the hypoxic pulmonary vascular response was measured in five calves anaesthetised with a combination of guaiacol, ketamine and xylazine. Alveolar hypoxia was induced by means of the inhalation of a gas mixture with an inspiratory oxygen fraction of 14-18 per cent. This alveolar hypoxia resulted in a pronounced puhnonary hypertension (mean pulmonary artery pressure in hypoxic animals : 30.2 mmHg). Inhalation of 20 and 40 ppm of nitric oxide significantly attenuated the hypoxia induced pulmonary hypertension. The effect ceased once nitric oxide administration was stopped. A concentration of 40 ppm of nitric oxide fully abolished the hypoxia induced pulmonary hypertension (mean pulmonary artery pressure during inhalation of 40 ppm nitric oxide : 22.8 mmHg). Inhalation of nitric oxide had no effect on systemic arterial blood pressure nor on systemic vascular resistance. It was concluded that inhalation of 20 or 40 ppm of nitric oxide prevented a selective pulmonary vasoconstriction during alveolar hypoxia in calves, which may he helpful in the treatment of acute respiratory disorders in calves.
The Journal of physiology, 1994
1. The actions of inhibitors of the release or action of nitric oxide (NO) on pulmonary vascular resistance (PVR) were investigated in lungs isolated from pig, sheep, dog and man. 2. In pig, sheep and human lungs perfused with Krebs-dextran solution, both N omega-nitro-L-arginine methyl ester (L-NAME; 10(-5) M) and Methylene Blue (10(-4) M) increased basal PVR. This increase was reversed by sodium nitroprusside (10(-5) M). In pig lungs N omega-monomethyl-L-arginine (10(-4) M) increased PVR by 154%. This increase was partially reversed by L-arginine (10(-3) M). L-NAME had no effect in dog lungs. 3. Pulmonary artery pressure-flow (PPA/Q) relationships were studied over a wide range of flows. In pigs, sheep and human lungs perfused with Krebs-dextran solution, L-NAME increased the PPA/Q slope. This increase was reversed by sodium nitroprusside. In dog lungs L-NAME had no effect. 4. In blood-perfused lungs, the respective responses to L-NAME were similar to those observed with saline. A...
European Journal of Anaesthesiology, 1996
Summary intravenous nitroglycerine, inhaled nitric oxide increased arterial PaO 2 from 5.3 to 5.9 kPa (P=0.02). Pulmonary hypertension is usually treated with intra-Both treatments diminished central venous pressure venous (i.v.) vasodilators, but their use is limited by and left atrial pressure, suggesting a possible cardiac systemic effects. In the current study, we compared effect. Inhaled nitric oxide was shown to be a potent the effects of inhaled nitric oxide and intravenous pulmonary vasodilator which attenuated pulmonary nitroglycerine on pulmonary and systemic haemohypertension and improved arterial oxygenation withdynamic responses as well as on gas exchange measout important direct effects on systemic pressure in urements in anaesthetized pigs whose pulmonary porcine hypoxia-induced pulmonary hypertension. pressure was increased by hypoxia (FiO 2 =15%). Both treatments reduced pulmonary pressure to the control Keywords: nitric oxide, nitroglycerine, pulmonary hylevel. Inhaled nitric oxide did not affect systemic arpertension, systemic arterial pressure, cardiac effect, terial pressure but intravenous nitroglycerine depig. creased it from 126.2 to 108.8 mmHg (P=0.04). Unlike
Journal of Pediatric Surgery, 1994
Inhaled nitric oxide (NO) is effective as a selective pulmonary vasodilator, but its effects on uninjured lungs subjected to normoxia and hypoxia have not been fully studied. The authors sought the response of pulmonary vascular resistance (PVR) to inhaled NO in piglet lungs devoid of ischemic injury in a model of reversible pulmonary hypertension. If the changes were dose-responsive, the authors asked whether the PVR changes were related to normoxia or hypoxia, and hypothesized that the change would be more pronounced for hypoxia than normoxia. In situ isolated piglet lungs were prepared by occlusive tracheostomy and ligation of the ductus arteriosus and aorta. Cannulae positioned in the left atrium and pulmonary artery were connected to a standard extracorporeal membrane oxygenation (ECMO) circuit, and flow was increased to approximate cardiac output. After stabilization, piglets (aged 5 to 14 days, weighing 3.2 to 6.4 kg) were divided into two groups of four each: normoxic (FIO2 0.30, normal PVR) and hypoxic (FIO2 0.07, increased PVR). NO was administered at 10 to 80 parts per million (ppm) in increments of 10 ppm, for 5 minutes at each concentration, with a return to baseline before each new dose. Flow, pulmonary arterial (PA) and left atrial (LA) pressures were continuously monitored, from which PVR was calculated (PVR = [PPA - PLA]/flow) and expressed as log delta PVR. Data were analyzed statistically by repeated measures of analysis of variance, comparing log delta PVR to baseline at each dose of NO, and comparing log delta PVR for normoxic and hypoxic lungs at each dose of NO.(ABSTRACT TRUNCATED AT 250 WORDS)
British Journal of Anaesthesia, 1999
Inhaled nitric oxide, a selective pulmonary vasodilator, is known to improve arterial oxygenation after cardiopulmonary bypass and during acute respiratory distress syndrome in humans. During general anaesthesia with spontaneous ventilation, healthy adult horses develop large alveolar-arterial oxygen tension differences. In this study, we have determined the effects of inhaled nitric oxide (10 parts per million (ppm)) on venous admixture and pulmonary haemodynamics in horses anaesthetized with halothane. Seven adult horses were studied twice in random sequence. After premedication with romifidine 100 µg kg -1 , anaesthesia was induced with ketamine 2.2 mg kg -1 and maintained with 1.1 MAC (0.95%) of halothane in oxygen. Horses breathed spontaneously. After 65 min, each horse had nitric oxide 10 ppm added to the inspired gas for 20 min (procedure HAϩNO) or anaesthesia was continued with halothane in oxygen (procedure HA). Cardiac output, minute ventilation, arterial and mixed venous oxygen and carbon dioxide tensions, and mean pulmonary and carotid arterial pressures were measured for 100 min. Shunt fraction and pulmonary and systemic vascular resistances were calculated. Shunt fraction (SF) and mean pulmonary artery pressure (P PA mean ) were not different between the two groups after 65 min of general anaesthesia (HA: SF 0.20 (SD 0.06), P PA mean 45 (8) mm Hg; HAϩNO: SF 0.21 (0.04), P PA mean 44 (7) mm Hg) or after 85 min (HA: SF 0.22 (0.07), P PA mean 45 (8) mm Hg; HAϩNO: SF 0.20 (0.03), P PA mean 43 (7) mm Hg). There were no significant effects of time or nitric oxide inhalation on any other variable. There was a significant correlation (rϭ0.80, PϽ 0.05) between calculated shunt fraction 65 min after induction of anaesthesia and body weight. 1999; 83: 321-4
Circulation, 1999
Background-We compared the hemodynamic responses to inhibition or stimulation of endothelial nitric oxide (NO) release of isolated explanted lungs from transplantation recipients with pulmonary hypertension and in normotensive unallocated donor lungs. Methods and Results-Lungs from 10 patients with severe pulmonary hypertension (SPH) and from 16 patients with severe chronic obstructive lung disease (COLD) were studied. Fourteen normotensive lungs were studied as controls. The lungs were perfused at a constant flow. In protocol 1 N G -nitro-L-arginine methyl ester caused a similar rise in baseline pulmonary artery pressure (PAP) that was similar in SPH (ϩ17.1Ϯ4.2 mm Hg; nϭ5), COLD (ϩ15.5Ϯ4.8 mm Hg; nϭ8), and control lungs (ϩ14.5Ϯ1.5 mm Hg; nϭ7). Arterial occlusion demonstrated that most of the changes with N G -nitro-L-arginine methyl ester were precapillary. The response to sodium nitroprusside (10 Ϫ8 to 10 Ϫ4 mol/L) was similar in all groups. In protocol 2, the lungs were preconstricted, and acetylcholine (10 Ϫ9 to 10 Ϫ5 mol/L) caused a lesser fall in PAP in both COLD and SPH lungs compared with control (Ϫ41.9Ϯ8.6%, Ϫ55.7Ϯ7.6%, and Ϫ73.2Ϯ2.5%, respectively; PϽ0.05), whereas sodium nitroprusside (10 Ϫ5 mol/L) decreased PAP to initial levels in all lungs. Conclusions-Stimulated release of NO is impaired in arteries of lungs with plexogenic or hypoxemic pulmonary hypertension. In contrast, basal release of NO appears to be maintained. (Circulation. 1999;100:1316-1321.)