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- W155403193 abstract "Thermally injured children who have sustained inhalation injury show evidence of restrictive lung disease during their recovery period. We hypothesize that lung arginase activity is increased by burn and inhalation injury, leading to increased collagen deposition in the lung and contributing to long-term pulmonary dysfunction. METHODS Ewes were randomly divided into (1) Uninjured: n=6 and (2) injured: n=7 groups. The injured animals were subjected to 20% TBSA burn and 36 breaths of cotton smoke under deep anesthesia. RESULTS DDAH-II, an enzyme that degrades ADMA, which is an endogenous inhibitor of NOS, significantly decreases after 2 and 3 weeks in the lung compared with uninjured animals. Lung ADMA increases from 2 to 3 weeks. Expression of iNOS significantly decreases in the lung 2 weeks after injury compared with uninjured animals. Lung arginase activity and hydroxyproline, a marker of collagen deposition, increase with 3 weeks post-injury compared to the uninjured animals. The increases in arginase and collagen are associated with reduced gas exchange and lung diffusion capacity after 3 weeks compared to uninjured animals. CONCLUSION The decrease in DDAH-II results in increased ADMA, resulting in decreased NOS. The decrease NOS causes an increase in arginase activity because NOS forms NOHA, which forms NO and inhibits arginase. The increase in arginase activity contributes to the increase in collagen deposition, which leads to long-term pulmonary dysfunction. Interruption of this pathological chain reaction may be useful in preventing the long-term sequelae of the smoke inhalation and burn injury." @default.
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- W155403193 date "2010-04-01" @default.
- W155403193 modified "2023-09-27" @default.
- W155403193 title "Lung arginase activity is increased in ovine model of acute lung injury and contributes to long term pulmonary dysfunction" @default.
- W155403193 doi "https://doi.org/10.1096/fasebj.24.1_supplement.984.11" @default.
- W155403193 hasPublicationYear "2010" @default.
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