Brain death disrupts structure and function of pig liver.

OBJECTIVE

To observe the effects of brain death on hepatic structure and function in pigs and to assess the role of nuclear factor kappaB (NF-kappaB).

MATERIALS AND METHODS

Twelve healthy pigs were randomly allocated to 2 groups of 6 each: a control group with Foley balloon catheter placement intracalvarium only, and a group with brain death established for 24 hours. Serum and hepatic tissue were obtained at 6, 12, and 24 hours after initial confirmation of brain death. Aspartate aminotransferase and alanine aminotransferase concentrations were determined using automated biochemistry analysis. Interleukin-1beta was determined using an enzyme-linked immunosorbent assay. The NF-kappaB messenger RNA was determined using real-time polymerase chain reaction, and NF-kappaB p65 using immunohistochemistry.

RESULTS

Concentrations of aspartate aminotransferase, alanine aminotransferase, and interleukin-1beta in serum, and NF-kappaB messenger RNA and NF-kappaB p65 in hepatic tissue were higher in the brain-dead group compared with the control group, and all increased over time (P<.05).

CONCLUSION

The NF-kappaB activated by brain death promotes synthesis and release of inflammatory mediators, resulting in hepatic dysfunction.