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Advances in the Pathogenesis of Adhesion Development

机译:黏附发展的发病机理研究进展

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摘要

Over the past several years, there has been increasing recognition that pathogenesis of adhesion development includes significant contributions of hypoxia induced at the site of surgery, the resulting oxidative stress, and the subsequent free radical production. Mitochondrial dysfunction generated by surgically induced tissue hypoxia and inflammation can lead to the production of reactive oxygen and nitrogen species as well as antioxidant enzymes such as superoxide dismutase, catalase, and glutathione peroxidase which when optimal have the potential to abrogate mitochondrial dysfunction and oxidative stress, preventing the cascade of events leading to the development of adhesions in injured peritoneum. There is a significant cross talk between the several processes leading to whether or not adhesions would eventually develop. Several of these processes present avenues for the development of measures that can help in abrogating adhesion formation or reformation after intraabdominal surgery.
机译:在过去的几年中,人们越来越认识到,粘连发展的发病机理包括在手术部位引起的缺氧,所产生的氧化应激以及随后的自由基产生的重要贡献。由外科手术引起的组织缺氧和炎症产生的线粒体功能障碍可导致活性氧和氮物种以及抗氧化酶(如超氧化物歧化酶,过氧化氢酶和谷胱甘肽过氧化物酶)的产生,这些酶在最佳状态下有可能消除线粒体功能障碍和氧化应激,预防导致受伤腹膜粘连发展的一系列事件。在这几个过程之间存在重大的串扰,最终导致是否最终形成粘附。这些过程中的几种为开发有助于消除腹腔内手术后粘连形成或再形成的措施提供了途径。

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