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L-NAME aggravates pulmonary oxygen toxicity in rats
G Capellier1, V Maupoil, A Boillot
1CHU Jean Minjoz, Besançon, France.
The European Respiratory Journal
|December 1, 1996
Summary
Inhibiting nitric oxide (NO) with NG-nitro-L-arginine methyl ester (L-NAME) worsened oxygen toxicity in rats, leading to earlier death and increased lung injury, suggesting NO is protective against hyperoxia.
Area of Science:
- Pulmonary Medicine
- Toxicology
- Biochemistry
Background:
- High oxygen concentration causes acute lung injury and death.
- Nitric oxide (NO) may protect against free radical damage.
- The role of NO in oxygen toxicity is not fully understood.
Purpose of the Study:
- To investigate the effect of NG-nitro-L-arginine methyl ester (L-NAME), a NO synthase inhibitor, on oxygen toxicity in rats.
- To determine if endogenous NO plays a protective role against hyperoxia-induced pulmonary lesions.
Main Methods:
- Rats were exposed to continuous high oxygen concentration.
- L-NAME (50 mg.kg-1) was administered intraperitoneally twice daily on the first day.
- Control groups received saline.
- Mortality, haematocrit, bronchoalveolar lavage fluid protein, lung water content, and plasma/lung TBARS were measured.
Main Results:
- L-NAME administration significantly increased mortality within 60 hours (57% vs. 22% in saline controls).
- Haematocrit and bronchoalveolar lavage fluid protein were significantly elevated in L-NAME treated rats.
- Lung water content was higher in oxygen-exposed groups and slightly decreased by L-NAME.
- Plasma TBARS increased, while lung TBARS decreased in oxygen-exposed animals, with no significant L-NAME effect.
Conclusions:
- NG-nitro-L-arginine methyl ester (L-NAME) had a deleterious effect in rats exposed to hyperoxia.
- Endogenous nitric oxide (NO) appears to have a protective role against hyperoxia-induced pulmonary lesions.
- Further research is warranted to elucidate the mechanisms of NO's protective effects.