Natural surfactant combined with superoxide dismutase and catalase decreases oxidative lung injury in the preterm lamb

2013 ◽  
Vol 49 (9) ◽  
pp. 898-904 ◽  
Author(s):  
Carlo Dani ◽  
Iuri Corsini ◽  
Mariangela Longini ◽  
Silvia Burchielli ◽  
Giulia Dichiara ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Lung Injury ◽  
Natural Surfactant

Natural surfactant combined with beclomethasone decreases oxidative lung injury in the preterm lamb

2009 ◽  
Vol 44 (12) ◽  
pp. 1159-1167 ◽  
Author(s):  
Carlo Dani ◽  
Iuri Corsini ◽  
Silvia Burchielli ◽  
Valentina Cangiamila ◽  
Mariangela Longini ◽  
...  
Keyword(s):  
Lung Injury ◽  
Natural Surfactant

Re-distribution of Superoxide Dismutase is Protective Against Acute Lung Injury in Staphylococcus aureus Pneumonia

2020 ◽  
Vol 159 ◽  
pp. S47
Author(s):  
Christina Sul ◽  
Laura Hernandez-Lagunas ◽  
Nana Burns ◽  
Michelle Brajcich ◽  
Christine Vohwinkel ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Superoxide Dismutase ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Staphylococcus Aureus Pneumonia

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.

Natural surfactant and hyperoxic lung injury in primates. II. Morphometric analyses

1994 ◽  
Vol 76 (3) ◽  
pp. 1002-1010 ◽  
Author(s):  
P. J. Fracica ◽  
S. P. Caminiti ◽  
C. A. Piantadosi ◽  
F. G. Duhaylongsod ◽  
J. D. Crapo ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Epithelial Cells ◽  
Lung Injury ◽  
Type I ◽  
Fibroblast Proliferation ◽  
Surfactant Treatment ◽  
Natural Surfactant ◽  
Hyperoxic Lung Injury ◽  
Diffuse Lung

Diffuse lung injury is accompanied by low compliance and hypoxemia with histological evidence of endothelial and alveolar epithelial cell disruption. The histological effects of treatment of an acute diffuse lung injury with a natural surfactant product were evaluated in a primate model because surfactant function and content have been shown to be abnormal in diffuse lung injury in both animals and humans. Ten baboons were ventilated with 100% O2 for 96 h, and 5 were given an aerosol of natural porcine surfactant. Physiological and biochemical measurements of the effects of hyperoxia and surfactant treatment are presented in a companion paper. After O2 exposure, lungs were fixed and processed for quantitative electron microscopy. The responses to O2 included epithelial and endothelial cell injuries, interstitial edema, and inflammation. The hyperoxic animals treated with surfactant were compared with the untreated animals; the treatments altered neutrophil distribution, fibroblast proliferation, and changes in the volumes of type I epithelial cells and endothelial cells. Surfactant-treated animals also had decreased lamellar body volume density in type II epithelial cells and preservation of endothelial cell integrity. These changes suggest complex effects of natural surfactant on the pulmonary response to hyperoxia, including protection against epithelial and endothelial cell destruction as well as significant interstitial inflammation and fibroblast proliferation. We conclude that natural surfactant treatment of hyperoxic lung injury in primates resulted in partial protection of epithelial and endothelial cells but also increased the accumulation of fibroblasts in the lung.

Superoxide dismutase potentiates platelet-activating factor-induced injury in perfused lung

1994 ◽  
Vol 266 (3) ◽  
pp. L246-L254 ◽  
Author(s):  
Y. C. Huang ◽  
E. S. Nozik ◽  
C. A. Piantadosi
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Hypertension ◽  
Superoxide Dismutase ◽  
Lung Injury ◽  
Platelet Activating Factor ◽  
Anion Channel ◽  
Lung Edema ◽  
Rabbit Lung ◽  
Edema Formation ◽  
Nitric Oxide Synthase Inhibitor

Platelet-activating factor (PAF) causes pulmonary hypertension and lung edema in animals and isolated perfused lungs by poorly understood mechanisms. Because oxidative mechanisms have been implicated in PAF-mediated cellular injury, we tested the hypothesis that superoxide anion (O2-.) contributes to PAF-induced lung injury by determining whether superoxide dismutase (SOD) could prevent the lung injury. Isolated rabbit lungs were perfused with PAF (100 nM) at a dose that caused transient hypertension and mild edema. Lungs pretreated with Cu,Zn SOD (100 U/ml) for 10 min developed persistent pulmonary hypertension and more lung edema formation in response to PAF. Enhanced responses to PAF also were observed in lungs perfused with 200 U/ml Cu,Zn SOD, but not with 10 or 40 U/ml Cu,Zn SOD. The higher doses of SOD also decreased thromboxane B2 levels in the perfusate. Potentiation of the PAF effect by Cu,Zn SOD was eliminated if the enzyme was inactivated or if the lung was treated with an anion channel blocker. The augmented PAF response in the presence of SOD was not altered by catalase (200 U/ml) or by nitric oxide synthase inhibitor. The data suggest that excessive Cu,Zn SOD enzyme activity potentiates PAF-induced injury in perfused rabbit lung presumably by overscavenging extracellular O2.- generated from intercellular sources. The augmented responses to PAF are not directly attributable to increased hydrogen peroxide, nitric oxide-related products, or thromboxane A2 production. These results suggest the new hypothesis that a balance between O2-. production and its metabolism determines vascular and endothelial responses to PAF.

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