THE EFFECT OF ANTITHROMBIN ON PULMONARY ENDOTHELIAL DAMAGE INDUCED BY CRUSH INJURY
THE EFFECT OF ANTITHROMBIN ON PULMONARY ENDOTHELIAL DAMAGE INDUCED BY CRUSH INJURY
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DOI：
10.1097/shk.0b013e3181a23ad0
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发表时间：
2009-12-01
期刊：
影响因子：
3.1
通讯作者：
Sugimoto, Hisashi
中科院分区：
文献类型：
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作者：
Sonoi, Hideaki;Matsumoto, Naoya;Sugimoto, Hisashi
挤压伤后，患者往往会出现多器官功能障碍综合征。在这项研究中，我们专注于血管内皮损伤，这被认为是多器官功能障碍综合征的一个可能原因，并揭示了一个病理条件的远端器官衰竭。特别是，肺是挤压伤后全身炎症侵袭时特别容易发生的靶器官。我们确定了抗凝血酶（AT）的作用，这是最近引起注意的内皮保护作用。使用大鼠挤压综合征模型，我们通过血液检查和肺损伤程度评估了全身炎症和血管内皮损伤的严重程度，并集中关注内皮随时间的形态学分析。挤压伤显著升高组织纤溶酶原激活物-纤溶酶原激活物抑制物1复合物、单核细胞趋化蛋白1和IL-6的血液浓度。释放挤压后24 h，肺内活跃炎性细胞（OX-42阳性细胞）的积聚以及血管性血友病因子和血管细胞粘附分子1的表达显著增加。48 h后肺泡结构紊乱，肺泡出血。抗凝血酶管理显着抑制炎症细胞的积累，血管性血友病因子和血管细胞粘附分子1的表达，和死亡率。我们的研究表明，挤压伤诱导急性肺损伤作为远端器官衰竭，它似乎是AT管理减少血管内皮损伤，并有效对抗挤压伤。
After crush injury, patients often experience multiple organ dysfunction syndrome. In this study, we focused on vascular endothelial damage, which is believed to be a possible cause of multiple organ dysfunction syndrome, and revealed a pathological condition of distant organ failure. In particular, the lung is an especially prone target organ at the time of systemic inflammatory invasion after crush injury. We ascertained the effect of antithrombin (AT), which has recently attracted attention for its endothelial protective effects. Using a rat model of crush syndrome, we assessed severity of systemic inflammation and vascular endothelial damage through a blood test and degree of lung injury and centrally focused on morphological analysis of endothelium over time. Crush injury significantly elevated the blood concentration of tissue plasminogen activator-plasminogen activator inhibitor 1 complex, monocyte chemoattractant protein 1, and IL-6. Accumulation of active inflammatory cells (OX-42-positive cells) and expression of von Willebrand factor and vascular cell adhesion molecule 1 significantly increased in the lung 24 h after releasing crush. After 48 h, disarray of alveolar structure and alveolar hemorrhage appeared. Antithrombin administration significantly suppressed accumulation of inflammatory cells, expression of von Willebrand factor and vascular cell adhesion molecule 1, and mortality rate. Our research demonstrates that crush injury induces acute lung injury as distant organ failure, and it would seem that AT administration diminishes vascular endothelial damage and is effective against crush injury.