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Lung trauma has been considered to be one of the vital injuries induced by explosion-generated blast overpressure. Conflicting evidence exists as to whether nitric oxide plays a crucial role in acute lung injury induced by blast. Data presented in this study demonstrate that local exposure of midthoracic region to moderate-level blast overpressure significantly enhanced lipid peroxidation product malondialdehyde and superoxide anion generation in rabbit's lungs 30 minutes after exposure, whereas the activities of antioxidant enzymes (superoxide dismutase, glutathione peroxidase) activity showed parallel increase. NG-nitro-L-arginine methyl ester, a non-specific inhibitor of nitric oxide synthase (NOS), had no effects on the measured parameters suggesting that oxidative stress induced by blast exposure might be independent from NOS

Oxidative stress in blast-induced acute lung injury is independent of enzymatic nitric oxide production