Oxidative stress due to activated neutrophils, macrophages and endothelial cells plays a crucial role in acute lung injury. This study compares the effects of the nonradical oxidants hypochlorite (HOCl) and hydrogen peroxide (H₂O₂) on pulmonary artery pressure [PAP (torr)], capillary filtration coefficient (K_f,c), tissue lipid peroxidation (LPO) and reduced glutathione (GSH) depletion. HOCl, H₂O₂ (1000 nmol min⁻¹) or buffer (control) is infused into isolated rabbit lungs. PAP, K_f,c and lung weight were measured. Experiments were terminated after 105 min or when fluid retention exceeded 50 g. Lung tissue was analyzed for LPO products and GSH. The oxidants induced comparable maximum effects. However, the patterns of lung injury were distinct: H₂O₂ infusion evoked an early biphasic pressure response (ΔPAP_max 2.8±0.22/4.2±0.37 after 5.7±1.4/39±4.0 min) and a sixfold increase in K_f,c after 90 min. HOCl application caused a late pressure response (ΔPAP_max 7.6±1.7 after 50.6±3.7 min) and a sevenfold increase in K_f,c after 60 min. H₂O₂-induced effects were attenuated by desferal. This may suggest an involvement of transition metal catalysed hydroxyl radical formation. Different oxidants induced distinct patterns of changes in PAP and K_f,c, which are accompanied by a comparable accumulation of LPO products and by a distinct degree of GSH depletion.