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  • Title: Hyperbaric oxygen increases the lung's susceptibility to inhaled lipopolysaccharide in mice.
    Author: Kang BH, Wan FJ, Chen TC, Huang KL, Tseng CJ.
    Journal: Lung; 2002; 180(2):105-17. PubMed ID: 12172903.
    Abstract:
    Hyperbaric oxygen (HBO2) has been shown to inhibit the adhesion function of beta(2)-integrin, which is important in mediating cell-to-cell adhesion and extravasation of inflammatory cells. In the present study, we examined the effects of HBO2 exposure on neutrophil infiltration and tissue injury in a model of acute lung inflammation induced by lipopolysaccharide (LPS) inhalation. Male C57BL/6 mice of 8 weeks old were exposed to 3 atmosphere absolute (ATA) 100% HBO2, 3 ATA hyperbaric air (HBA), or room air for 90 min. After exposure, they were exposed to aerosolized LPS solution (1 mg/ml) or saline in a plexiglass chamber for 10 min. Four hours after inhalation, bronchoalveolar lavage (BAL) was performed to determine protein concentration, LDH activity, total cells, and differential cell counts in the lavage fluid (BALF). Myeloperoxidase (MPO) content, lung histopathology, and plasma nitric oxide (NO) metabolite concentrations were also determined in separate sets of animals. We observed that LPS inhalation increased neutrophil number in the BALF, which was significantly inhibited by HBO2 but not HBA pre-exposure. However, MPO content in the lung was prominently increased by HBO2 pre-exposure, which correlated with increased PMN infiltration in lung tissues. Further, HBO2 plus LPS, but not saline inhalation caused a significant increase in the BALF protein level and LDH activity compared with that of LPS inhalation alone. LPS exposure induced significant increase in plasma NO metabolites, which was not potentiated by HBO2 pre-exposure. The inducible nitric oxide synthase inhibitor, aminoguanidine, significantly attenuated the increases in plasma NO metabolites and tissue MPO content as well as lung injuries. In summary, our data suggest that HBO2 pre-exposure increases the lung's susceptibility to inhaled LPS, which may be related to increased tissue neutrophil infiltration and dependent on interaction(s) between HBO2 exposure with LPS-induced nitric oxide production.
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