1. The effects of the scavengers of reactive oxygen species superoxide dismutase and catalase, the iron chelator desferrioxamine and the nitric oxide synthase inhibitor NG-nitro-l-arginine methyl ester and saline (control vehicle) on hypoxic pulmonary vasoconstriction, a measure of albumin flux and an index of lipid peroxidation (palmitic:linoleic acid ratio) were investigated after ischaemia—reperfusion in an isolated, blood-perfused rat lung model.

2. Lungs treated immediately before reperfusion with catalase (5 000 units), desferrioxamine (2 mg/kg), NG-nitro-l-arginine methyl ester (5 mmol/l) or saline showed a significant augmentation in pre-ischaemia—reperfusion hypoxic pulmonary vasoconstriction (57.7 ± 6.0%, 82.7 ± 28.8%, 95.2 ± 36.6% and 45.95 ± 10.53% respectively), an increase in albumin flux (0.35 ± 0.04, 0.31 ± 0.06, 0.29 ± 0.04 and 0.33 ± 0.02) and an increase in pre-ischaemia—reperfusion palmitic:linoleic acid ratio (0.64 ± 0.08, 0.51 ± 0.19, 0.5 ± 0.04 and 0.17 ± 0.07). Superoxide dismutase (2 750 i.u.) administered immediately before reperfusion prevented completely the changes in hypoxic pulmonary vasoconstriction (−0.3 ± 5.4%), albumin flux (0.09 ± 0.11) and palmitic:linoleic acid ratio (–0.06 ± 0.12). In control lungs (2 h of continuous perfusion), superoxide dismutase, catalase, desferrioxamine and saline did not affect hypoxic pulmonary vasoconstriction (5.5 ± 4.9%, 1.0 ± 3.1%, −5.1 ± 1.8% and 3.0 ± 6.6%). However, NG-nitro-l-arginine methyl ester significantly augmented hypoxic pulmonary vasoconstriction (275.1 ± 39.3%). There was no effect of superoxide dismutase, catalase, desferrioxamine, NG-nitro-l-arginine methyl ester or saline in control lungs on albumin flux (0.10 ± 0.04, 0.11 ± 0.01, 0.1 ± 0.01, 0.12 ± 0.01 and 0.11 ± 0.01 respectively) or palmitic:linoleic acid ratio (–0.08 ± 0.08, 0.73 ± 0.76, −0.03 ± 0.12, 0.01 ± 0.17 and 0.00 ± 0.0 respectively).

3. We conclude that superoxide dismutase attenuates ischaemia—reperfusion-induced increases in albumin flux and hypoxic pulmonary vasoconstriction, and prevents consumption of linoleic acid in the isolated, blood-perfused rat lung.

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