BACKGROUND Pulmonary air embolism (PAE) occurs in inappropriate decompressions or clinical complications. Sudden lodging of air bubbles in the pulmonary circulation results in pulmonary hypertension, pulmonary edema, and deficiency in cardiopulmonary functions, which are often fatal without timely intervention. In this study, we investigated the effectiveness of hyperbaric oxygen (HBO2) therapy on the acute lung injury induced by venous air infusion in rats. METHODS Systemic and pulmonary arterial pressures were monitered through catheters in the femoral artery and pulmonary artery, respectively. PAE was induced by venous infusion of air at the rate of 25 microL x min(-1). Wet/dry weight ratio of the lung and protein concentration and LDH activity in the bronchoalveolar lavage (BAL) fluid were measured at the end of the experiment. RESULTS Air infusion raised the mean pulmonary arterial pressure (MPAP) within 10 min to a plateau that was 208% above the baseline value. The wet/dry ratio of lungs were 4.83 +/- 0.28, 4.98 +/- 0.39, and 5.20 +/- 0.38 in the groups receiving 0.13, 0.50, and 1.0 ml of air infusion, respectively, which were significantly higher than the control group that averaged 4.47 +/- 0.24. The protein concentration (mg x L(-1)) and the LDH activity (mAbs x min(-1)) in BAL fluid increased from 291 +/- 78 and 21.6 +/- 4.8 in the control group to 1491 +/- 402 and 83.3 +/- 15.4, 1432 +/- 278 and 75.2 +/- 35.4, and 1809 +/- 493 and 59.6 +/- 23.3 in the lungs receiving air infusion for 5, 20, and 40 min, respectively. Treatment with hyperbaric oxygen at 3 ATA or 6 ATA, or with isoproterenol reduced neither the increased wet/dry weight ratio nor the protein concentration and LDH activity in the BAL fluid. CONCLUSIONS Our results demonstrated that venous air infusion induced acute lung injury in rats and suggested that neither HBO2 therapy nor isoproterenol treatment could not effectively reverse the PAE-induced lung injury.