CENTRILOBULAR INJURY FOLLOWING HYPOXIA IN ISOLATED, PERFUSED-RAT-LIVER
CENTRILOBULAR INJURY FOLLOWING HYPOXIA IN ISOLATED, PERFUSED-RAT-LIVER
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DOI：
10.1126/science.7256265
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发表时间：
1981-01-01
期刊：
影响因子：
56.9
通讯作者：
THURMAN, RG
中科院分区：
文献类型：
--
作者：
LEMASTERS, JJ;JI, S;THURMAN, RG
缺氧产生在隔离，无血红蛋白，灌注大鼠肝脏通过减少进入器官的O2携带液的流速。该手术导致小叶中心区域缺氧。在这些缺氧区域，结构紊乱迅速发展，其特征是肝细胞质膜通过窦状内皮中的开窗形成水泡样突起。门静脉周围组织保持含氧量正常，完全幸免。局部缺氧引起的细胞损伤可能在小叶中心型肝病的发病机制中起重要作用。
Hypoxia was produced in isolated, Hb-free, perfused rat liver by reducing the flow rate of O2-carrying fluid entering the organ. The procedure caused anoxia in centrilobular regions. In these anoxic areas, structural derangements developed rapidly, characterized by bleb-like protrusions of hepatocyte plasma membrane through fenestrations in the sinusoidal endothelium. Periportal tissue remained normoxic and was completely spared. Cellular injury resulting from localized anoxia may play an important role in the pathogenesis of centrilobular liver disease.