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首页> 外文期刊>Surgical Endoscopy >Renal oxidative stress following CO2 pneumoperitoneum-like conditions.
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Renal oxidative stress following CO2 pneumoperitoneum-like conditions.

机译：类似于CO2气腹的条件后的肾脏氧化应激。

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BACKGROUND: Physiologic renal changes associated with pneumoperitoneum (PNP) have been described and various underlying mechanisms have been suggested. We investigated the possibility that PNP-associated renal damage is pressure dependent, and that oxidative stress is thereby involved. MATERIALS AND METHODS: Seventy Wistar rat kidneys (n=10 per group) were isolated. They were perfused with oxygenated, warm, Krebs-Henseleit solution containing 5% albumin within an isolated environment and subjected to various CO(2) pressures (0 [control], 3, 5, 8, 12, 15, and 18 mmHg) for 60 min. Half of each group was additionally perfused for 30 min at 0 mmHg pressure. RESULTS: Renal flow decreased proportionately to the applied pressure as did urine output: both decreased (P < 0.05) after 60 and 90 min when pressure >or=8 mmHg was applied. Oxygen extraction decreased (P<0.05) during PNP in all pressurized groups. Xanthine oxidase (XO) activity and reduced glutathione in the tissues increased (P<0.05) proportionately to pressures >or=8 mmHg. All parameters slightly reversed toward baseline values, upon the release of the intra-chamber pressure, except for the 18 mmHg group's values. CONCLUSIONS: CO(2)-PNP pressure induces kidney injury, possibly reversible immediately after pressure is annulled. Pressure is associated with oxidative stress, which interferes with cellular metabolism and function, possibly via an ischemic-reperfusion-like mechanism.
机译：背景：已经描述了与气腹（PNP）有关的生理性肾脏变化，并提出了各种潜在的机制。我们调查了与PNP相关的肾脏损害与压力有关的可能性，并因此涉及了氧化应激。材料与方法：分离出70只Wistar大鼠肾脏（每组n = 10）。在隔离的环境中，向它们灌注含5％白蛋白的含氧温暖Krebs-Henseleit溶液，并使其经受各种CO（2）压力（0 [对照]，3、5、8、12、15和18 mmHg） 60分钟每组的一半另外在0mmHg压力下灌注30分钟。结果：肾流量与所施加的压力成比例地降低，尿量也一样：当施加压力≥8mmHg时，在60和90分钟后两者均降低（P <0.05）。在所有加压组中，PNP期间的氧提取均下降（P <0.05）。组织中的黄嘌呤氧化酶（XO）活性和减少的谷胱甘肽与压力大于或等于8 mmHg的比例成比例地增加（P <0.05）。释放腔内压力后，除18 mmHg组的所有值外，所有参数均略微向基线值反转。结论：CO（2）-PNP压力可引起肾脏损伤，可能在压力消除后立即可逆。压力与氧化应激有关，氧化应激可能通过缺血再灌注样机制干扰细胞的新陈代谢和功能。

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