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.