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Alveolar acid transiently permeabilizes the alveolar epithelium in mouse lungs
Author(s) -
Lindert Jens,
Bhattacharya Jahar
Publication year - 2011
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.25.1_supplement.865.7
Subject(s) - fluorescence microscope , chemistry , alveolar epithelium , biophysics , fluorescence , cytosol , membrane , lung , pulmonary alveolus , fluorophore , respiratory system , pathology , epithelium , anatomy , biochemistry , biology , medicine , macrophage , in vitro , physics , enzyme , quantum mechanics
Acid aspiration causes acute lung injury (ALI). However, acid interactions with the alveolar epithelial (AE) membrane are not understood. To understand acid interactions with intact alveoli, we set up isolated, perfused mouse lungs held at pulmonary artery, left atrial and alveolar pressures of 10, 3 and 5 cmH 2 O, respectively. Then we imaged intact alveoli by real‐time fluorescence microscopy. To view the alveolar cytosol, we microinfused alveoli with BCECF‐AM, that intra‐cellularly converts to the membrane‐impermeable fluorophore, BCECF. Then we imaged pH‐independent fluorescence (440 nm excitation). Alveolar microinfusion of HCl (pH 1.5) decreased AE fluorescence by 48±7 % of initial in 5 min (mean±SE, n=3). However subsequently, despite continued HCl infusion for 15 min, the AE fluorescence held steady. Further, after reloading BCECF to initial levels of AE fluorescence, a second HCl infusion given 20 min after the first, failed to decrease AE fluorescence (p<.05). We conclude, first contact with acid immediately permeabilized the AE membrane. However, the membrane spontaneously resealed and resisted further acid‐induced damage. We report a novel protective mechanism in ALI in which the cell spontaneously repairs chemically‐induced membrane damage. (Support: HL69514, 78645).