Objective      To investigate the therapeutic effect of L-arginine on phosgene-induced acute lung injury in rats.  Methods      Forty-eight male SD rats were randomized into 8 groups (n=6 per group): normal control group

phosgene exposure group

L-arginine control group

treatment groups with L-arginine at low

middle and high doses

dexamethasone treatment group and L-arginine plus dexamethasone treatment group. Except the normal control and L-arginine control groups

the other 6 groups were exposed to phosgene gas produced from 0.45 g triphosgene in a sealed cabin for 5 min. The L-arginine treatment

dexamethasone treatment

and control groups were intraperitoneally injected with L-arginine immediately after exposure

dexamethasone and saline

respectively. Lung function in each group were determined at 2

4 and 6 hours after the phosgene exposure. All rats were sacrificed at 6 h after exposure. The wet/dry ratio of the lung

contents of glutathione (GSH) and malondialdehyde (MDA)

activities of superoxide dismutase (SOD) and inducible nitric oxide synthase (iNOS) in plasma were measured

and pathological observation was performed on lung tissue under light microscope.  Results      Compared with the normal control group

the phosgene exposure group showed significant changes in lung function parameters. Meanwhile

significant increase of lung wet/dry ratio (P0.01)

MDA content (P0.01) and iNOS activity (P0.05)

as well as significant decrease of GSH content and SOD activity (P0.05) in plasma were detected. Compared with the phosgene exposure group

lung function parameters were improved in the L-arginine treatment groups

accompanying with significantly decreased MDA content and iNOS activity

as well as significantly increased GSH content and SOD activity

The dexamethasone treatment group showed significantly decreased MDA content (P0.05)

increased SOD activity (P0.05)

but the changes in wet/dry ratio of the lung

GSH content and iNOS activity in plasma were not significant.  Conclusion      L-arginine has protective effect on phosgeneinduced lung injury

and its protective mechanism may be associated with scavenging of free radicals and iNOS inhibition.