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脂质过氧化不是灌注肺中水肿形成的主要因素。

Lipid peroxidation is not a major factor involved in the edema formation in perfused lungs.

作者信息

Risberg B, Smith L, Schoenberg M H, Younes M

出版信息

Eur Surg Res. 1987;19(3):164-70. doi: 10.1159/000128696.

Abstract

Perfusion of isolated rat lungs was previously found to induce edema formation, which was considered to be mediated by oxygen-free radicals as scavengers reduced the edema. In the present study we elaborated upon these findings by measuring products found by O2-radical generation. We measured reduced and oxidized glutathione as well as conjugated dienes as an estimate of lipid peroxidation. Amount of water was also measured. Perfusion with oxygenated dextran/Tyrode solution increased edema as compared to nonoxygenated dextran/Tyrode and to nonperfused control lungs. Induction of oxygen radical formation by addition of xanthine and xanthine oxidase to the nonoxygenated dextran/Tyrode perfusate significantly increased the amount of edema as measured by the percentage of water in the lung to 87.0% as compared to the control value of 78.2%. Addition of the radical scavenger superoxide dismutase and catalase to this perfusate prevented edema accumulation. Levels of conjugated dienes as well as those of reduced and oxidized glutathione in lung tissue were measured before the start of perfusion and after 5 and 30 min of perfusion. No significant changes were seen in any of these parameters, indicating that lipid peroxidation may not be a major factor contributing to the edema formation during perfusion of isolated lungs.

摘要

先前发现,对离体大鼠肺进行灌注会导致肺水肿形成,这种肺水肿被认为是由氧自由基介导的,因为清除剂可减轻水肿。在本研究中,我们通过测量由氧自由基生成所产生的产物来详细阐述这些发现。我们测量了还原型和氧化型谷胱甘肽以及共轭二烯,以评估脂质过氧化作用。还测量了水的含量。与未充氧的右旋糖酐/台氏液以及未灌注的对照肺相比,用充氧的右旋糖酐/台氏液进行灌注会增加肺水肿。向未充氧的右旋糖酐/台氏液灌注液中添加黄嘌呤和黄嘌呤氧化酶以诱导氧自由基形成,与对照值78.2%相比,通过肺中水分百分比测量的水肿量显著增加至87.0%。向该灌注液中添加自由基清除剂超氧化物歧化酶和过氧化氢酶可防止水肿积聚。在灌注开始前以及灌注5分钟和30分钟后,测量了肺组织中共轭二烯以及还原型和氧化型谷胱甘肽的水平。这些参数均未观察到显著变化,这表明脂质过氧化作用可能不是离体肺灌注过程中导致肺水肿形成的主要因素。

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