Increased Nitric Oxide Biosynthesis in Leukotoxin,9,10-Epoxy-12-Octadecenoate Injured Lung

We measured effluent nitric oxide levels using a chemiluminescence method from leukotoxin (Lx, a linoleate epoxide) injured isolated rat lungs perfused with physiological salt solution. Nitric oxide production from Lx-injured lung promptly increased and lasted for 20 min. Pretreatment with NG-monome...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 1995-05, Vol.210 (1), p.133-137
Main Authors: Ishizaki, T., Shigemori, K., Yamamura, Y., Matsukawa, S., Nakai, T., Miyabo, S., Hayakawa, M., Ozawa, T., Voelkel, N.F.
Format: Article
Language:English
Subjects:
Animals
Arginine - analogs & derivatives
Arginine - pharmacology
Edema - chemically induced
Linoleic Acids - pharmacology
Lung - drug effects
Lung - metabolism
Male
Nitric Oxide - metabolism
omega-N-Methylarginine
Rats
Rats, Sprague-Dawley
Time Factors
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Summary:We measured effluent nitric oxide levels using a chemiluminescence method from leukotoxin (Lx, a linoleate epoxide) injured isolated rat lungs perfused with physiological salt solution. Nitric oxide production from Lx-injured lung promptly increased and lasted for 20 min. Pretreatment with NG-monomethyl-L-arginine (LNMMA) significantly suppressed Lx-induced production of nitric oxide. Effluent from control lungs showed trace levels of nitric oxide. The wet to dry lung weight (WLW/DLW) after termination of the experiments was significantly elevated in Lx-treated lungs compared with that of LNMMA pretreated lungs or control lungs. There was a correlation between nitric oxide levels (at 10 min) and lung edema (WLW/DLW). Thus, nitric oxide plays a role in the pathogenesis of Lx-induced lung injury.
ISSN:0006-291X
1090-2104
DOI:10.1006/bbrc.1995.1637