坏死
肝细胞
程序性细胞死亡
细胞凋亡
缺血
微循环
正弦波
细胞外
生物
管腔(解剖学)
再灌注损伤
细胞外基质
灌注
男科
内皮干细胞
高架桥
病理
医学
内科学
细胞生物学
生物化学
体外
作者
Pierre‐Michel Huet,Márcia Regina Nagaoka,Geneviève Desbiens,Esther Tarrab,Antoine Brault,Marie‐Pierre Bralet,Marc Bilodeau
出处
期刊:Hepatology
[Wiley]
日期:2004-03-25
卷期号:39 (4): 1110-1119
被引量:119
摘要
Cold ischemia-warm reperfusion (CI-WR) injury of the liver is characterized by marked alterations of sinusoidal endothelial cells (SECs), whereas hepatocytes appear to be relatively unscathed. However, the time course and mechanism of cell death remain controversial: early versus late phenomenon, necrosis versus apoptosis? We describe the occurrence and nature of cell death after different periods of CI with University of Wisconsin (UW) solution and after different periods of WR in the isolated perfused rat liver model. After 24- and 42-hour CI (viable and nonviable livers, respectively), similar patterns of liver cell death were seen: SEC necrosis appeared early after WR (10 minutes) and remained stable for up to 120 minutes. After 30 minutes of WR, apoptosis increased progressively with WR length. Based on morphological criteria, apoptotic cells were mainly hepatocytes within liver plates or extruded in the sinusoidal lumen. In addition, only after 42-hour CI were large clusters of necrotic hepatocytes found in areas of congested sinusoids. In these same livers, the hepatic microcirculation, evaluated by means of the multiple-indicator dilution technique, revealed extracellular matrix disappearance with no-flow areas. In conclusion, different time courses and mechanisms of cell death occur in rat livers after CI-WR, with early SEC necrosis followed by delayed hepatocyte apoptosis. These processes do not appear to be of major importance in the mechanism of graft failure because they are similar under both nonlethal and lethal conditions; this is not the case for the loss of the extracellular matrix found only under lethal conditions and associated with hepatocyte necrosis.
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