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Inhibition of alveolar liquid secretion by lipopolysaccharide
Author(s) -
Lindert Jens,
Islam Mohammad N.,
Bhattacharya Jahar
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.762.6
Subject(s) - secretion , chemistry , lipopolysaccharide , pulmonary surfactant , saline , lung , endocrinology , medicine , biochemistry
In the adult lung, the surfactant subphase formed by the alveolar wall liquid (AWL) determines alveolar patency. We reported that the AWL is established by alveolar liquid secretion (Am J Resp Cell Mol Biol. 2007. 36:688–96). To determine whether lung inflammation affects AWL secretion, we intra‐tracheally instilled saline or lipopolysaccharide (LPS) (1 mg/kg) in lungs of anesthetized rats. After 24h we isolated the lungs and perfused (14 ml/min) them at constant pressures of 10, 3 and 5 cmH2O held at respectively, the pulmonary artery, the left atrium and the airway. Then, we viewed the lungs by two‐photon microscopy. To determine AWL secretion rate ( J AWL ), we micropunctured single alveoli and microinfused FITC‐dextran (20 kD) to fluorescently label the AWL. We quantified FITC fluorescence in the AWL in 0.6 μm optical sections. In saline‐treated lungs AWL fluorescence intensity decreased exponentially to 61±3 % of initial in 20 min (mean±SE, n=3, P<.05), reflecting progressive fluorophore dilution by alveolar secretion. From the exponential regression of the fluorescence decay, we determined J AWL as 4.8±0.7 x10 −8 ml/(cm 2 .sec). However, in LPS‐instilled lungs J AWL was zero (n=3, P<.05), indicating absence of liquid secretion. We suggest that in septic lungs, impaired AWL secretion might underlie surfactant dysfunction, thereby impairing lung function. (HL78645, HL64896).