Hyperbaric oxygen attenuates lipoplysaccharide-induced acute lung injury

Objectives: To study the effect of hyperbaric oxygen therapy in alleviating acute lung injury induced by lipopolysaccharide (LPS) in rats. Design and interventions: The rats received an intraperitoneal injection of LPS (15 mg/kg). Animals were either breathing air at I ATA or subjected to hyperbaric oxygen (HBO2) therapy. The HBO2 therapy was carried out in a hyperbaric chamber at a pressure of 3 ATA for 90 min. In another two groups, LPS-treated rats also received intraperitoneal injection of N-omega-nitro-L-arginine (LNAME, 25 mg/kg) or L-N-6-(iminoethyl)lysine (LNIL, 10 ml/kg). Another two groups of LPS-treated rats were subjected to HBO2 exposure after the injection of L-NAME or L-NIL. Measurements and main results: The bronchoalveolar lavage (BAL) was done into the left lung at 7.5 h after intraperitoneal injection of LPS. Parts of the right lung were excised for myeloperoxidase measurement, whereas the rest was collected for wet/dry ratio determination. LPS significantly increased the nitrite/nitrate (NOx-) concentration (34.4+/-15.7 vs 4.5+/-3.1 muM), LDH activity (66+/-17 vs 46+/-15 mAbs/min), and protein concentration (373+/-119 vs 180+/-90 mg/l) in the BAL fluid. Treatment with HBO2 immediately after the injection of LPS enhanced the increase of NOx- production, but reduced the LDH and protein in BAL fluid to the control levels. Pretreatment with either L-NAME or L-NIL abolished the increase of NOx- in the BAL fluid and further elevated the LDH level and protein concentration. Conclusion: Our results suggested that HBO2 alleviates the LPS-induced acute lung injury, which may be related to the enhancement of nitric oxide production.