Effect of Hypotensive Brain Death on the Donor Liver and Its Mechanism in an Improved Bama Miniature Pig (Sus scrofa domestica) Model.

BACKGROUND

We aimed to observe the effect of hypotensive brain death on the donor liver and understand its pathophysiological mechanism in improved pig model.

METHODS

The model was induced using the modified intracranial water sac inflation method in 16 Bama miniature pigs. Effects of hypotensive brain death on liver function and tissue morphology were evaluated via changes in liver function enzyme index, liver tissue alkaline phosphatase levels, hourly bile flow, and liver tissue pathology. Its pathophysiological mechanism was examined on the basis of changes in portal vein blood flow, hepatic artery blood flow, portal venous endotoxin level, and liver tissue cytokine levels.

RESULTS

After model establishment, portal vein blood flow, hepatic arterial blood flow, hourly bile flow, and alkaline phosphatase content in hepatic tissue significantly decreased, and serum aspartate aminotransferase, alkaline phosphatase, and lactate dehydrogenase levels significantly increased. Hematoxylin-eosin staining of liver tissue showed that after model establishment, hepatic tissue injury was gradually aggravated and hepatic cells were irreversibly damaged at 7 hours. Portal vein endotoxin levels significantly increased after brain death. Tumor necrosis factor α, interleukin 1, and endothelin 1 levels in liver tissues significantly increased at 3, 6, and 12 hours after brain death (P < .05), and hypoxia-inducible factor 1-α and nitric oxide levels significantly decreased (P < .05).

CONCLUSIONS

Hepatic injury was progressively aggravated under hypotensive brain death. The mechanism of donor liver injury under hypotensive brain death may involve low liver perfusion, release of intestinal endotoxin and inflammatory factors (eg, tumor necrosis factor α and interleukin 1), decreased hypoxia-inducible factor 1-α, and endothelin 1 and nitric oxide imbalance.