Chinese Journal of Tissue Engineering Research ›› 2010, Vol. 14 ›› Issue (53): 9905-9908.doi: 10.3969/j.issn.1673-8225.2010.53.006

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Protective effect of prostaglandin E1 on hepatic microcirculation in brain death rats

Wu Lin-wei, Guo Zhi-yong, Tai Qiang, Ju Wei-qiang, Wang Dong-ping, He Xiao-shun   

  1. Department of Organ Transplantation, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou  510080, Guangdong Province, China
  • Online:2010-12-31 Published:2010-12-31
  • Contact: He Xiao-shun, Doctor, Professor, Department of Organ Transplantation, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, Guangdong Province, China gdtrc@163.com
  • About author:Wu Lin-wei☆, Doctor, Attending physician, Department of Organ Transplantation, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, Guangdong Province, China lw97002@163.com
  • Supported by:

    the Science and Technology Plan of Guangdong Province, No. 2008B030301308*

Abstract:

BACKGROUND: Brain death donor management has an important role on protecting the function of organs. Prostaglandin E1 (PGE1) is used widely in the filed of liver transplantation because of its effect on protecting the liver function, but its effect on the brain death donors and the grafts has not been illustrated.
OBJECTIVE: To investigate the protective effect of PGE1 on hepatic microcirculation in brain death donor rats models.
METHODS: Sprague-Dawley rats were inducted brain death by gradual on-set method. All rats were divided into 3 groups: brain death group, PGE1 group and contrast group. Blood and liver specimen were harvested at 2 and 4 hours after brain death induction. The activities of aspartate aminotransferase and alanine aminotransferase were detected by automatic biochemical analyzer, hyaluronic acid (HA) concentration was measured by radio immunoassay, and the ultrastructure changes of hepatic sinusoid were observed by Hitachi H-600 transmission electron microscope.
RESULTS AND CONCLUSION: Hepatic function was dysfuncted at 2 hours after brain death, which aggravated at 4 hours. Liver enzymes in the PGE1 group were improved compared with the brain death group (P < 0.05). At 2 hours after brain death, HA levels were increased in the brain death group at 2 hours and continuous rose at 4 hours. After brain death, electron microscope showed the microstructure of the hepatocytes and sinusoids endothelial cells were damaged, Kupffer cells were activated. PGE1 management on the brain death donor can improve the microcirculation of liver, inhibit apoptosis of liver cells and activation of Kupffer cells, and then it can improve the quality of liver grafts from brain death donors.

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