Extracorporeal membrane oxygenation (ECMO) therapy can result in systemic immune inflammation and trigger a hemolytic response, both of which can lead to oxidative stress injury. However, currently, there are few studies about whether ECMO can lead to oxidative stress injury. The objective of this study was to determine the effect of ECMO therapy on systemic oxidative stress. Twelve pigs were randomly divided into control and ECMO treatment groups. Blood samples were collected at -1, 0, 2, 6, 12, and 24 h during ECMO therapy in order to measure the levels of various oxidative stress markers in plasma. All animals included in the study were euthanized after 24 h of ECMO treatment. Malondialdehyde (MDA) was used as a marker of oxidation, and superoxide dismutase (SOD), glutathione (GSH), and total antioxidant capacity (T-AOC) were used as indices for antioxidant activity. The plasma levels of each molecule were similar when measured at -1 and 0 h (P > 0.05). In the control group, MDA, SOD, GSH, and T-AOC remained relatively constant throughout the study period. However, when ECMO was administered for 2 h, plasma levels of MDA increased significantly; conversely, levels of SOD, GSH, and T-AOC decreased. Maximum MDA levels and minimal SOD, GSH, and T-AOC levels were observed after 6 h of ECMO treatment. MDA and SOD levels had returned to baseline at 24 h. At this time-point, levels of MDA and T-AOC in samples from the right frontal cortex and jejunum differed significantly between the control and ECMO treatment groups. These results show that early ECMO treatment can induce significant oxidative stress injury in plasma. However, in the latter stage of the treatment, the oxidative stress injury can be repaired gradually. ECMO treatment can also result in mild oxidative stress injury in the jejunum and brain tissue.
Keywords: Acute respiratory distress syndrome; Extracorporeal membrane oxygenation; Immune inflammation; Oxidative stress.
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