国际麻醉学与复苏杂志   2013, Issue (4): 8-8
    
失血性休克急性肺损伤的发病机制
徐睿, 李启芳, 姜虹1()
1.上海交通大学附属第九人民医院
Recent development on the athogenesis of acute lung injury induced by hemorrhagic shock
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摘要：

背景　急性肺损伤（acute lung injury， ALI）是失血性休克死亡率和发病率升高的重要原因。　目的　对失血性休克ALI的可能发病机制作一综述。　内容　多核中性粒细胞（ polymorph nuclear neutrophils， PMNs），Toll样受体（Toll-like receptors， TLRs），活性氧（Reactive Oxygen Species， ROS），低氧诱导因子（hypoxia-inducibie factor， HIF）以及核因子（nuclear factor-κB， NF-κB）的激活和相互作用参与了创伤失血性休克后ALI，并且发挥了关键作用。　趋势　加深对创伤失血性休克ALI发病机制和各种损伤因素横向联系将有助于其治疗。
关键词： 急性肺损伤；创伤；失血性休克；Toll样受体；低氧诱导因子
Abstract:

Background Acute lung injury (ALI) is an important cause for mortality and morbidity of patients with traumatic hemorrhagic shock. Objective To provide a review about the possible pathogenesis of ALI induced by traumatic hemorrhagic shock. Content Activity and interaction of polymorph nuclear neutrophils（PMNs）, Toll-like receptors（TLRs）, hypoxia-inducibic factor（HIF） and nuclear factor-κB（NF-κB） are involved in the pathogenesis of ALI induced by traumatic hemorrhagic shocks, and play important roles. Trend To study the pathogenesis of ALI induced by traumatic hemorrhagic shock and the interaction of injury factors will contribute to the treatment of this disorder.
Key words: Acute lung injury； Trauma； Hemorrhagic shock； Toll-like receptors； Hypoxia-inducibic factor