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Oxidative stress in lung tissue induced by CO(2) pneumoperitoneum in the rat.

机译:CO(2)气腹在大鼠中诱导的肺组织中的氧化应激。

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BACKGROUND: Clinical trials have found that the pneumoperitoneum has potentially hazardous side effects. The biochemical basis of organ injury induced by pneumoperitoneum is, however, not well defined. Since oxidative stress is believed to play an important role in many pathological conditions, we set out to examine oxidative stress markers in the lung, liver, kidney, and pancreas by using a rat model of laparoscopy with CO(2) pneumoperitoneum and comparing it to a group with gasless laparoscopy. METHODS: Malondialdehyde (for lipid peroxidation), protein-bound carbonyls (for protein oxidation), reduced and oxidized glutathione, and the neutrophil marker myeloperoxidase were evaluated in tissue homogenates at 2 h, 6 h, and 18 h after laparoscopy. Immunoblotting was used to analyze the modification of lung proteins by 4-hydroxynonenal at 6 h. RESULTS: Significant lipid peroxidation was found selectively in lungs at 2 h and 6 h after CO(2) pneumoperitoneum. This was accompanied by a loss of glutathione but only minor protein oxidation. Further, lung proteins were clearly modified by the aldehydic product of lipid peroxidation 4-hydroxynonenal. Myeloperoxidase in lungs increased continuously up to 18 h in both experimental groups, but there were higher levels in the group with pneumoperitoneum. CONCLUSION: Oxidative stress is likely to contribute to the impairment of pulmonary function after laparoscopic operations using a CO(2) pneumoperitoneum.
机译:背景:临床试验发现气腹具有潜在的有害副作用。然而,由气腹引起的器官损伤的生化基础尚不明确。由于氧化应激被认为在许多病理状况中都起着重要的作用,因此我们着手使用腹腔镜与CO(2)气腹的大鼠模型并通过比较将其与肺,肝,肾和胰腺中的氧化应激标志物进行比较。一组无气腹腔镜。方法:在腹腔镜检查后2 h,6 h和18 h的组织匀浆中评估丙二醛(用于脂质过氧化),蛋白质结合的羰基(用于蛋白质氧化),还原型和氧化型谷胱甘肽以及中性粒细胞标记过氧化物酶。使用免疫印迹分析了6小时时4-羟基壬烯醛对肺蛋白的修饰。结果:CO(2)气腹后2 h和6 h在肺中选择性地发现了明显的脂质过氧化作用。这伴随着谷胱甘肽的损失,但是仅有少量的蛋白质氧化。此外,脂质过氧化4-羟基壬烯醛的醛产物明显修饰了肺蛋白。在两个实验组中,肺过氧化物酶在18 h内均持续增加,但在气腹组中,其水平更高。结论:氧化应激可能会导致腹腔镜手术使用CO(2)气腹后肺功能的损害。

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