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

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

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

A251 THE EFFECT OF INHALED NITRIC OXIDE DURING PARTIAL LIQUID VENTILATION IN THE RABBIT OLEIC ACID LUNG INJURY MODEL

1997 ◽  
Vol 87 (Supplement) ◽  
pp. 251A
Author(s):  
Tokujiro Uchida ◽  
Koichi Nakazawa ◽  
Koshi Makita ◽  
Kuninori Yokoyama ◽  
Keisuke Amaha
Keyword(s):  
Nitric Oxide ◽  
Oleic Acid ◽  
Lung Injury ◽  
Inhaled Nitric Oxide ◽  
Partial Liquid Ventilation ◽  
Liquid Ventilation ◽  
Injury Model ◽  
Lung Injury Model
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