Inhaled Nitric Oxide Selectively Reduces Pulmonary Hypertension After Ovine Smoke Inhalation But Does Not Improve Oxygenation

Booke, Michael; Bradford, Darien W.; Hinder, Frank; Nishida, Katsumi; Biondo, Nettie; Traber, Lillian D.; Traber, Daniel L.

doi:10.1097/00004630-199701000-00005

Cited by 20 publications

(8 citation statements)

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“…Direct measurement of NO is difficult due to the very short half-life [29]. However, the stable oxidation end product of NO production, nitrite, can be readily measured in biological fluids and has been used in vitro and in vivo as an indicator of NO production [30].…”

Section: Methodsmentioning

confidence: 99%

Inhibition of c-Jun NH2-terminal kinase or extracellular signal-regulated kinase improves lung injury

et al. 2004

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Section: Methodsmentioning

confidence: 99%

Inhibition of c-Jun NH2-terminal kinase or extracellular signal-regulated kinase improves lung injury

et al. 2004

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“…NO concentrations in the supernatants of alveolar macrophage cultures were measured by using a nitrite assay. Direct measurement of NO is difficult due to the very short half-life (23). However, the stable oxidation end-product of NO production, nitrite, can be readily measured in biological fluids and has been used in vitro and in vivo as an indicator of NO production (24).…”

Section: Methodsmentioning

confidence: 99%

Time course for inhibition of lipopolysaccharide-induced lung injury by genistein: Relationship to alteration in nuclear factor-κB activity and inflammatory agents*

Kang

Lee²,

Lee³

et al. 2003

Critical Care Medicine

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This study reports the time course of the inhibitory effects of a single genistein pretreatment on acute lung injury with the maximal effects at 4 hrs after lipopolysaccharide treatment. However, a multiple dosing schedule with genistein retained the inhibitory effect on acute lung injury at 24 hrs after lipopolysaccharide treatment. The mechanisms by which genistein exerts an inhibitory effect on acute lung injury may involve the suppression of nuclear factor-kappaB activation, matrix metalloproteinase-9 activity, and NO production.

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“…[25][26][27][28][29][30][31][32][33] However, the dose-dependent response to inhaled NO in human trials has been inconsistent. [34][35][36][37][38][39][40][41] In addition, there are few data on the potential interactions between traditional pulmonary vasodilating therapies, i.e., hyperoxia and alkalosis, and the dosing of inhaled NO. 41 The purpose of the present study was to determine the potential dose-response interactions between inhaled NO and hyperoxia, and between inhaled NO and alkalosis in an experimental model of acute pulmonary hypertension.…”

Section: Introductionmentioning

confidence: 99%

Inhaled nitric oxide, oxygen, and alkalosis: Dose-response interactions in a lamb model of pulmonary hypertension

et al. 1999

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Inhaled nitric oxide (NO) is currently used as an adjuvant therapy for a variety of pulmonary hypertensive disorders. In both animal and human studies, inhaled NO induces selective, dose‐dependent pulmonary vasodilation. However, its potential interactions with other simultaneously used pulmonary vasodilator therapies have not been studied. Therefore, the objective of this study was to determine the potential dose‐response interactions of inhaled NO, oxygen, and alkalosis therapies. Fourteen newborn lambs (age 1–6 days) were instrumented to measure vascular pressures and left pulmonary artery blood flow. After recovery, the lambs were sedated and mechanically ventilated. During steady‐state pulmonary hypertension induced by U46619 (a thromboxane A2 mimic), the lambs were exposed to the following conditions: Protocol A, inhaled NO (0, 5, 40, and 80 ppm) and inspired oxygen concentrations (FiO2) of 0.21, 0.50, and 1.00; and Protocol B, inhaled NO (0, 5, 40, and 80 ppm) and arterial pH levels of 7.30, 7.40, 7.50, and 7.60. Each condition (in randomly chosen order) was maintained for 10 min, and all variables were allowed to return to baseline between conditions. Inhaled NO, oxygen, and alkalosis produced dose‐dependent decreases in mean pulmonary arterial pressures (P < 0.05). Systemic arterial pressure remained unchanged. At 5 ppm of inhaled NO, alkalosis and oxygen induced further dose‐dependent decreases in mean pulmonary arterial pressures (P<0.05). At inhaled NO doses >5 ppm, alkalosis induced further dose‐independent decreases in mean pulmonary arterial pressure, while oxygen did not. We conclude that in this animal model, oxygen, alkalosis, and inhaled NO induced selective, dose‐dependent pulmonary vasodilation. However, when combined, a systemic arterial pH >7.40 augmented inhaled NO‐induced pulmonary vasodilation, while an FiO2 >0.5 did not. Therefore, weaning high FiO2 during inhaled NO therapy should be considered, since it may not diminish the pulmonary vasodilating effects. Further studies are warranted to guide the clinical weaning strategies of these pulmonary vasodilator therapies. Pediatr Pulmonol. 1999; 28:3–11. © 1999 Wiley‐Liss, Inc.

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Inhaled Nitric Oxide Selectively Reduces Pulmonary Hypertension After Ovine Smoke Inhalation But Does Not Improve Oxygenation

Cited by 20 publications

References 0 publications

Inhibition of c-Jun NH2-terminal kinase or extracellular signal-regulated kinase improves lung injury

Inhibition of c-Jun NH2-terminal kinase or extracellular signal-regulated kinase improves lung injury

Time course for inhibition of lipopolysaccharide-induced lung injury by genistein: Relationship to alteration in nuclear factor-κB activity and inflammatory agents*

Inhaled nitric oxide, oxygen, and alkalosis: Dose-response interactions in a lamb model of pulmonary hypertension

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