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肝缺血再灌注不同时限细胞凋亡和增殖变化的动态研究
引用本文:李德忠,卢绮萍. 肝缺血再灌注不同时限细胞凋亡和增殖变化的动态研究[J]. 华南国防医学杂志, 2005, 19(2): 19-22
作者姓名:李德忠  卢绮萍
作者单位:广州军区武汉总医院电镜室,武汉,430070;广州军区武汉总医院普通外科
基金项目:国家自然科学基金资助项目 (39770938)
摘    要:目的 探讨肝完全缺血后再灌注不同时限肝细胞凋亡和增殖发生发展的动态变化,为临床肝脏手术时抗损伤处理提供实验依据。方法实验以假手术组为对照;应用FCM检测及透射电镜技术对SD大鼠肝缺血30min再灌注0,0.5,1,3,6.12,24,48,72,96h的肝细胞凋亡及增殖变化进行了动态观察。结果随再灌注时限的延续肝细胞呈现连续性的非典型性细胞凋亡和增殖反应病理变化。经历了潜伏期、急性期、交错期、和恢复期四个阶段。缺血再灌注诱发的肝细胞凋亡开始于急性期。可波及大多数肝细胞。但只有少数细胞发生凋亡,这些细胞在交错期病变加重,在恢复期死亡并逐渐被吞噬清除。而大部细胞则在急性期之后终止凋亡而向恢复结构与功能的途径发展。结论在短时间缺血后、再灌注可诱发少数肝细胞凋亡。大多数肝细胞经历短暂的凋亡前期反应后则进入恢复阶段,最终结果是肝脏结构和功能的恢复。

关 键 词:肝脏  缺血再灌注  细胞凋亡  超微结构
修稿时间:2004-11-17

Dynamic Studies of Hepatocyte Apoptosis and Proliferation Induced by Ischemia- Reperfusion
LI De-zhog,LU Qi-ping. Dynamic Studies of Hepatocyte Apoptosis and Proliferation Induced by Ischemia- Reperfusion[J]. Military Medical Journal of South China, 2005, 19(2): 19-22
Authors:LI De-zhog  LU Qi-ping
Affiliation:LI De-zhog,LU Qi-ping . Electron Microscope Laboratoty,General Surgical Department,Wuhan General Hospital,PLA,Wuhan Hubei,430070,China
Abstract:Objective To provide experiment evidence for treating the liver damage induced by ischemia-reperfusion in liver's surgical operation, .Methods The reperfusion was performed 30 minutes after ischemia in the livers of the rats.The liver tissues of the experimental groups were taken at 0, 0.5, l, 3, 6, 12, 24, 48, 72 and 96 hours respectively after the reperfusion and the control group was treated with pseudo-operation. The hepatocytes apoptosis and proliferation induced by ischemia-reperfusion were dynamically determined by FCM and electron microscope. Results There was only a low apoptotic peak after 48 hours of reperfusion, but the proliferation of the liver cells began at 6 hours , reached the highest at 24 hours and returnedto normal level at 96 hours after the reperfusion. The liver cells shown a continuous nontypical apoptotic process in ultrastructural pathology as the period of reperfusion prolonged. There were four stages in the process, that is, incubation, acute, altemative and recovery stages. Although the apoptosis emerged at acute stage and involved the great majority of hepatocytes, morphological apoptotsis occurred only in a few cells where apoptosis became more serious in alterntive stage and death occurred in recovery stage and they finaly were engulfed by liver and kupffer cells. Their apoptosis process stopped and their ultrastrultures and fuctions began on return to normal after the acute stage in the great majority of the hepatocytes . Conclusion After short period ischemia, the reperfusion may induce nontypical apoptotic changes in a few liver cells, the majority of the cells get into recovery stage after the short damage reaction, and the return of their structures and functions to normal will be reached.
Keywords:Liver  Ischemia-reperfusion  Apoptosis  Ultrastuctural Pathology
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