scholarly journals Inhaled Nitric Oxide Attenuates Hyperoxic Lung Injury in Lambs

2006 ◽  
Vol 59 (1) ◽  
pp. 142-146 ◽  
Author(s):  
Robert B Cotton ◽  
Håkan W Sundell ◽  
Darryl C Zeldin ◽  
Jason D Morrow ◽  
L Jackson Roberts ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Lung Injury ◽  
Inhaled Nitric Oxide ◽  
Hyperoxic Lung Injury

Inhaled nitric oxide attenuates pulmonary inflammation and fibrin deposition and prolongs survival in neonatal hyperoxic lung injury

2007 ◽  
Vol 293 (1) ◽  
pp. L35-L44 ◽  
Author(s):  
Simone A. J. ter Horst ◽  
Frans J. Walther ◽  
Ben J. H. M. Poorthuis ◽  
Pieter S. Hiemstra ◽  
Gerry T. M. Wagenaar
Keyword(s):  
Nitric Oxide ◽  
Lung Injury ◽  
Mrna Expression ◽  
Plasminogen Activator ◽  
Growth Factor Receptor ◽  
Inhaled Nitric Oxide ◽  
Lung Pathology ◽  
Fibrin Deposition ◽  
Plasminogen Activator Inhibitor 1 ◽  
Hyperoxic Lung Injury

Administration of inhaled nitric oxide (iNO) is a potential therapeutic strategy to prevent bronchopulmonary dysplasia (BPD) in premature newborns with respiratory distress syndrome. We evaluated this approach in a rat model, in which premature pups were exposed to room air, hyperoxia, or a combination of hyperoxia and NO (8.5 and 17 ppm). We investigated the anti-inflammatory effects of prolonged iNO therapy by studying survival, histopathology, fibrin deposition, and differential mRNA expression (real-time RT-PCR) of key genes involved in the development of BPD. iNO therapy prolonged median survival 1.5 days ( P = 0.0003), reduced fibrin deposition in a dosage-dependent way up to 4.3-fold ( P < 0.001), improved alveolar development by reducing septal thickness, and reduced the influx of leukocytes. Analysis of mRNA expression revealed an iNO-induced downregulation of genes involved in inflammation (IL-6, cytokine-induced neutrophilic chemoattractant-1, and amphiregulin), coagulation, fibrinolysis (plasminogen activator inhibitor 1 and urokinase-type plasminogen activator receptor), cell cycle regulation (p21), and an upregulation of fibroblast growth factor receptor-4 (alveolar formation). We conclude that iNO therapy improves lung pathology and prolongs survival by reducing septum thickness, inhibiting inflammation, and reducing alveolar fibrin deposition in premature rat pups with neonatal hyperoxic lung injury.

Inhaled nitric oxide reduces lung edema during fluid resuscitation in ovine acute lung injury

2003 ◽  
Vol 29 (10) ◽  
pp. 1790-1797 ◽  
Author(s):  
Henning D. Stubbe ◽  
Martin Westphal ◽  
Hugo Van Aken ◽  
Christoph Hucklenbruch ◽  
Stefan Lauer ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Fluid Resuscitation ◽  
Inhaled Nitric Oxide ◽  
Lung Edema

scholarly journals Modulation of Pulmonary Cytochrome P4501A1 Expression by Hyperoxia and Inhaled Nitric Oxide in the Newborn Rat: Implications for Lung Injury

2006 ◽  
Vol 59 (3) ◽  
pp. 401-406 ◽  
Author(s):  
Xanthi I Couroucli ◽  
Yan-Hong Wei ◽  
Weiwu Jiang ◽  
Kathirvel Muthiah ◽  
Lee W Evey ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Lung Injury ◽  
Inhaled Nitric Oxide ◽  
Newborn Rat ◽  
Cytochrome P4501a1

Recombinant human superoxide dismutase reduces lung injury caused by inhaled nitric oxide and hyperoxia

1997 ◽  
Vol 272 (5) ◽  
pp. L903-L907 ◽  
Author(s):  
C. G. Robbins ◽  
S. Horowitz ◽  
T. A. Merritt ◽  
A. Kheiter ◽  
J. Tierney ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Superoxide Dismutase ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Lung Tissue ◽  
Pulmonary Inflammation ◽  
Inhaled Nitric Oxide ◽  
Newborn Piglets ◽  
Markers Of Inflammation ◽  
Cell Counts

We previously demonstrated that 48 h of 100 ppm inhaled nitric oxide (NO) and 90% O2 causes surfactant dysfunction and pulmonary inflammation in mechanically ventilated newborn piglets. Because peroxynitrite (the product of NO and superoxide) is thought to play a major role in the injury process, recombinant human superoxide dismutase (rhSOD, a scavenger of superoxide) might minimize this insult. Four groups of newborn piglets (1-3 days of age) were ventilated with 100 ppm NO and 90% O2 for 48 h. Piglets received no drug, 5 mg/kg rhSOD intratracheally at time 0, 5 mg/kg rhSOD intratracheally at 0 and 24 h, or 10 mg/kg rhSOD by nebulization at time 0. At 48 h, bronchoalveolar lavage (BAL) was performed, and lung tissue was analyzed for markers of inflammation, oxidative injury, acute lung injury, and surfactant function. There were significant differences between rhSOD-treated piglets and untreated controls with respect to BAL neutrophil chemotactic activity, cell counts, and protein concentration as well as lung tissue malondialdehyde concentrations. Minimum surface tension of BAL surfactant from all groups studied was increased, with no differences found among groups. These data suggest that rhSOD, at the doses used, mitigated the inflammatory changes, oxidative damage, and acute lung injury from exposure to 100 ppm NO and 90% O2 but did not appear to improve surfactant function. This has important clinical implications for infants treated with hyperoxia and NO for neonatal lung disorders.

Response to Inhaled Nitric Oxide in Acute Lung Injury Depends on Distribution of Pulmonary Blood Flow Prior to Its Administration

1999 ◽  
Vol 159 (2) ◽  
pp. 563-570 ◽  
Author(s):  
RENÉ GUST ◽  
TIMOTHY J. McCARTHY ◽  
JAMES KOZLOWSKI ◽  
ALAN H. STEPHENSON ◽  
DANIEL P. SCHUSTER
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Pulmonary Blood Flow ◽  
Inhaled Nitric Oxide
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