Donor pre-treatment with inhaled nitric oxide attenuates acute lung injury following single lung transplantation

1999 ◽  
Vol 18 (1) ◽  
pp. 78
Author(s):  
C.D. Sudarshan ◽  
H. Orr ◽  
S.C. Clark ◽  
J. Roughan ◽  
P. Flecknell ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Lung Transplantation ◽  
Inhaled Nitric Oxide ◽  
Single Lung Transplantation ◽  
Pre Treatment

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

Endotoxin alters the response to inhaled nitric oxide in acute lung injury

2000 ◽  
Vol 17 (Supplement 20) ◽  
pp. 4
Author(s):  
R. Gust ◽  
J. Kozlowski ◽  
T. J. McCarthy ◽  
D. P. Schuster
Keyword(s):  
Nitric Oxide ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Inhaled Nitric Oxide

Mitigation of endotoxin-induced acute lung injury in ventilated rabbits by surfactant and inhaled nitric oxide

2000 ◽  
Vol 26 (2) ◽  
pp. 229-238 ◽  
Author(s):  
D. H. Zhao ◽  
B. Sun ◽  
Z. H. Wu ◽  
R. Lindwall ◽  
B. Robertson
Keyword(s):  
Nitric Oxide ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Inhaled Nitric Oxide
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