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Chinese Journal of Hepatic Surgery(Electronic Edition) ›› 2013, Vol. 02 ›› Issue (05): 322-326. doi: 10.3877/cma.j.issn.2095-3232.2013.05.012

Special Issue:

• Basic Research • Previous Articles     Next Articles

Mechanism of liver injury of rabbits after brain death

Zi-biao ZHONG1, Qi-fa YE1,(), Xiao-li FAN1, Ling LI1, Yan-feng WANG1   

  1. 1. Institute of Hepatobiliary Diseases of Wuhan University, Zhongnan Hospital of Wuhan University, Transplant Medical Center of Wuhan University, Wuhan 430071, China
  • Received:2013-05-14 Online:2013-10-10 Published:2013-10-10
  • Contact: Qi-fa YE
  • About author:
    Corresponding author: YE Qi-fa, Email:

Abstract:

Objective

To explore the mechanism of liver injury of rabbits after brain death.

Methods

Sixty healthy male New Zealand rabbits were randomly divided into brain death group (n=30) and sham group (n=30) according to the random number table. Rabbits in brain death group were put to brain death by cranial drilling, cathetering and increasing intracranial pressure in a slow, intermittent way. While rabbits in sham group underwent cranial drilling and cathetering without pressuring. Ten rabbits from each group were respectively put to death at the time points of 2, 6, 8 h after operation, and the samples of blood and liver tissues were collected. Serum indexes of liver function were detected by colorimetry. Morphology change of liver was observed by haematoxylin-eosin (HE) staining. The levels of interleukin (IL)-1β and tumor necrosis factor (TNF)-α were detected by enzyme linked immunosorbent assay (ELISA). The difference between two groups was compared using t test and the difference of each time points within the group was compared using variance analysis and LSD-t test.

Results

The level of serum alanine aminotransferase (ALT) at 8 h after operation in brain death group was significant higher than that at 6 h after operation [(83±7)U/L vs. (52±4)U/L; LSD-t=29.65, P<0.05]. Liver edema and inflammatory cell infiltration in the portal area aggravated gradually in brain death group as time passed, neutrophil microabscess was observed at 8 h after operation and liver cell damage was found unobvious. While rabbits in sham group were found mainly with neutrophil infiltration. The level of serum IL-1β at 8 h after operation increased evidently in brain death group than that in sham group, and significant difference was observed [(46±5)mg/L vs. (33±4)mg/L; t=3.334, P<0.05]. The level of serum TNF-α at the time points of 2, 6, 8 h after operation increased evidently in brain death group than that in sham group, and significant difference was observed [(35.3±4.0)mg/L vs. (25.4±3.1)mg/L, (43.4±6.9) mg/L vs. (24.2±7.1)mg/L, (49.3±5.4)mg/L vs. (25.4±2.0)mg/L; t=3.409, 3.369, 7.224, P<0.05].

Conclusions

No obvious changes were observed in the liver function and morphology in brain death rabbits within 8 h after operation. Neutrophil microabscess and lymphocyte infiltration in the portal area were observed at 8 h after operation, which might be relevant with immunologic injury. It is ideal for donors of brain death rabbits to undergo liver transplantation within 8 h.

Key words: Brain death, Rabbit, Liver function tests, Tumor necrosis factor-alpha, Interleukin-1, Liver transplantation

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