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Updated: Aug 21, 2026
Brain Death Induction in Mice Using Intra-Arterial Blood Pressure Monitoring and Ventilation via Tracheostomy
Published on: April 17, 2020
The influence of brain death on liver in rats
1Institute of Transplantation, Tongji Hospital, Huazhong University of Science & Technology, Wuhan, People's Republic of China. zhangshuijun@zzu.edu.cn
Objective:
Donor brain death produces functional and morphological changes in peripheral organs. We examined the influence of brain death on liver function.
Methods:
Fifty rats were randomly divided into three groups: controls (C), sham-operated (E1), and brain-dead (E2). All rats underwent tracheotomy with assisted respiration. The sera of rats at 1 and 3 hours after brain death were tested for the levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), hyaluronic acid (HA), and endothelin-1 (ET-1). At the end of assisted respiration, liver samples were collected for ultrastructural observation.
Results:
At 1 and 3 hours, the levels of ALT, AST, HA, and ET-1 in group E2 were significantly higher than those in groups C and E1 (P < .05). The levels of ALT, AST, HA, and ET1 at 3 hours were significantly higher than those at 1 hour (P < .05). Under the electronic microscope, Kupffer cells were activated, sinusoidal endothelial cells (SEC) denuded, fenestration widened, and hepatocytes under the SEC exposed in group E2. In group C and E1, Kupffer cells were not obviously activated and SEC were almost intact.
Conclusions:
Brain death damages hepatocytes and nonparenchymal cells in rat. Endothelin-1 and Kupffer cells play an important role in the process. The clearance of hyaluronic acid may provide reliable index to judge SEC function after brain death.
