DO SPLANCHNIC VISCERA CONTRIBUTE TO LIVER PRESERVATION REPERFUSION INJURY

Preservation-reperfusion injury of hepatic allografts is thought to be associated with Kupffer cell activation and TNF release from the tran splanted organ. Confirmation that the allograft is the source of this TNF in an in vivo model is difficult because of rapid equilibration of this cytokine into all compartments. A novel experimental design was devised to aid in accurate localization of the site of TNF release fol lowing a orthotopic liver transplant (OLT). In the first group (anhepa tic), livers were removed from rats and splanchnic and systemic venous returns were then reestablished using a conduit of donor IVC and port al vein with a portasystemic shunt. In the second group (asplanchnic), the liver, stomach, pancreas, and intestine of the recipient were rem oved and a donor liver was reimplanted using the recipient IVC as the source of portal blood. The third (OLT-16) and fourth (OLT 8) groups u nderwent standard OLT with preservation times of 16 and 8 hr in 4 degr ees C Euro-Collins solution, respectively. TNF levels were significant ly increased in the OLT-16 group compared with the OLT-8 group. There were modest elevations of TNF in the anhepatic model, but the TNF in t he asplanchnic model appreached baseline. Absence of TNF in the asplan chnic group and a rise in TNF levels in the anhepatic group to that no t significantly different from OLT-16 or OLT-8 suggest that a major so urce of TNF following preservation reperfusion may be the intestine.