Ischemic preconditioning:: A defense mechanism against the reactive oxygen species generated after hepatic ischemia reperfusion
Ischemic preconditioning:: A defense mechanism against the reactive oxygen species generated after hepatic ischemia reperfusion
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DOI：
10.1097/00007890-200204270-00004
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发表时间：
2002-04-27
期刊：
影响因子：
6.2
通讯作者：
Roselló-Catafau, J
中科院分区：
文献类型：
--
作者：
Peralta, C;Bulbena, O;Roselló-Catafau, J
背景预处理对肝缺血再灌注（I/R）后的肝和肺损伤均有保护作用。黄嘌呤和黄嘌呤氧化酶（XOD）可能有助于肝I/R的发展。目的探讨预处理是否能减轻肝缺血再灌注后黄嘌呤/XOD对肝和肺的损伤作用。在大鼠I/R前诱导肝1111或预处理。测定肝脏和血浆中黄嘌呤和黄嘌呤脱氢酶/黄嘌呤氧化酶（XDH/XOD）的含量。评价肝损伤和肺部炎症反应。预处理可减少持续性缺血时肝脏中黄嘌呤的积累和XDH向XOD的转化。这可以减少由XOD产生的活性氧（ROS），从而减轻肝I/R损伤。抑制XOD可防止缺血后ROS的产生和肝损伤。黄嘌呤和XOD预处理大鼠的管理导致肝MDA和转氨酶水平类似于肝I/R后发现。预处理，导致低循环水平的黄嘌呤和XOD活性，减少中性粒细胞的积累，氧化应激和微血管疾病后，在肝脏I/R肺。抑制XOD可减轻肝I/R后肺组织的炎性损伤。给予黄嘌呤和XOD可消除预处理对肺损伤的益处。预处理通过阻断ROS产生的黄嘌呤/XOD途径，可保护肝脏免受I/R诱导的肝和肺损伤。
Background. Preconditioning protects against both liver and lung damage after hepatic ischemia-reperfusion (I/R). Xanthine and xanthine oxidase (XOD) may contribute to the development of hepatic I/R.Objective. To evaluate whether preconditioning could modulate the injurious effects of xanthine/XOD on the liver and lung after hepatic I/R.Methods. Hepatic 1111 or preconditioning previous to I/R was induced in rats. Xanthine and xanthine dehydrogenase/xanthine oxidase (XDH/XOD) in liver and plasma were measured. Hepatic injury and inflammatory response in the lung was evaluated.Results. Preconditioning reduced xanthine accumulation and conversion of XDH to XOD in liver during sustained ischemia. This could reduce the generation of reactive oxygen species (ROS) from XOD, and therefore, attenuate hepatic I/R injury. Inhibition of XOD prevented postischemic ROS generation and hepatic injury. Administration of xanthine and XOD to preconditioned rats led to hepatic MDA and transaminase levels similar to those found after hepatic I/R. Preconditioning, resulting in low circulating levels of xanthine and XOD activity, reduced neutrophil accumulation, oxidative stress, and microvascular disorders seen in lung after hepatic I/R. Inhibition of XOD attenuated the inflammatory damage in lung after hepatic I/R. Administration of xanthine and XOD abolished the benefits of preconditioning on lung damage.Conclusions. Preconditioning, by blocking the xanthine/XOD pathway for ROS generation, would confer protection against the liver and lung injuries induced by hepatic I/R.