The role of oxidative stress and effect of alpha-lipoic acid in reexpansion pulmonary edema – an experimental study

INTRODUCTION: We investigated the role of oxidative stress in the pathogenesis of reexpansion pulmonary edema (RPE) and effect of alpha-lipoic acid (ALA) in the prevention of RPE. MATERIAL AND METHODS: There were 4 groups consisting of 10 rats in each group; control group (CG), α-lipoic acid group (ALAG), reexpansion pulmonary edema group (RPEG), reexpansion pulmonary edema plus α-lipoic acid group (RPE + ALAG). In all the groups, all rats were sacrificed 2 hours after the reexpansion of lungs. To indicate oxidative stress malondialdehyde (MDA), and to indicate antioxidant status superoxide dismutase (SOD), catalase (CAT) and glutathione peroxides (GPx) were measured in the lungs of rats. RESULTS: Mean MDA value was lower in CG (7.02 ±0.14) and in ALAG (6.95 ±0.11) than the other groups (p = 0.001). It was highest in RPEG (8.89 ±0.21) (p = 0.001). It was lower in RPE + ALA G (7.21 ±0.32) than RPEG (p = 0.001). Antioxidant levels: GPx (37.21 ±3.01), CAT (2.87 ±0.14) and SOD (100.12 ±12.39) were lowest in RPEG among all groups (p = 0.001). These values were GPx (45.21 ±3.54), CAT (3.24 ±0.21) and SOD (172.36 ±15.48) in RPE + ALA G and were greater than those of RPEG (p = 0.001). While normal pulmonary parenchyma was seen in 2 rats in RPE + ALAG, it was not seen in RPEG. Pulmonary edema was seen in 1 rat in RPE + ALAG; however, it was seen in 3 in RPEG. CONCLUSIONS: Oxidative stress might have an important role in the pathogenesis of RPE. In addition, ALA treatment might contribute in preventing RPE.