Objective        To observe the changes of oxidative stress in the occurrence of pulmonary edema in rats induced by hypoxia and to investigate the pathophysiological significance.        Methods        A total of 72 adult male SD rats weighting 200±20 g were randomly divided into control group (C)

and simulated altitude acute hypoxia groups (H). The hypoxia group rats were exposed to a simulated altitude of 6 000 m  for 6

12

24

48 and 72 h respectively. The lung wet/dry (W/D) ratio

total-antioxidant capacity (T-AOC)

malondialdehyde (MDA) content

activity of superoxide dismutase (SOD) and catalase (CAT) were measured. Lung and plasma IL-6 were measured by ELISA.       Results        The W/D ratio was increased in hypoxia groups than in control group (H6

H12 and H24 vs C

P0.01

H48 and H72 vs C

P0.05). MDA content was gradually increased with the prolongation of hypoxia time

and reached the highest in 72 h after hypoxic exposure （P0.01）. SOD content was significantly deceased in 12 and 24 h after hypoxic exposure（P0.05） and further reduced in 48 and 72 h（P0.01）. Contents of T-AOC and CAT were significantly reduced with the prolongation of hypoxia time in 24

48 and 72 h（P0.05）. Plasma IL-6 was significantly increased in hypoxic 24

48 and 72 h groups （P0.01）

while that in lung tissue was significantly increased in hypoxic 48 and 72 h groups compared with the control group（H48 vs C

P0.01; H72 vs C

P0.05）.       Conclusion       Acute hypoxia-induced high altitude pulmonary edema is related to oxidative stress. Decrease of antioxidant capacity and increase of free radicals contribute to the occurrence of high altitude pulmonary edema.