During BD, liver-specific parameters (portal venous flow, microperfusion, aspartate aminotransferase activity, ENC, and hepatic oxidative stress) were compromised, independent of the hemodynamic status. Therefore, the systemic hemodynamic status does not reflect the functional status of the liver during BD.

Lymphoid and dendritic cells of donor origin can be detected in the recipient several years after a solid organ transplantation. This phenomenon is termed microchimerism and could play a role in the induction of tolerance. The fate of other hematopoietic cells transferred by liver transplantation, in particular of stem and progenitor cells, is unknown. For this reason, we studied peripheral blood and bone marrow samples of 12 patients who had received a liver transplant from an HLA-DR mismatched donor. Eight patients were long-term survivors between 2.8 and 10.1 years after allografting. CD34+ cells from bone marrow were highly enriched with the use of a 2-step method, and a nested polymerase chain reaction was applied to detect donor cells on the basis of allelic differences of the HLA-DRB1 gene. Rigorous controls with DRB1 specificities equal to the donor and host were included. In 5 of 8 long-term liver recipients, donor-specific CD34+ cells could be detected in bone marrow. Microchimerism in the CD34+ cell fraction did not correlate to the chimeric status in peripheral blood. In conclusion, our results demonstrate a frequent microchimerism among bone marrow–derived CD34+ cells after liver transplantation. The functional role of this phenomenon still needs to be defined.

The study was designed to concentrations were significantly assess the gastrointestinal ischaemia lower in the pretreated group and the influence of the specific [39 f 23 pg/ml (Control): 14 f 7 Kupffer cell toxin gadolinium chlo-(GdCI,); P < 0.051 suggesting an imride (GdC1,) on the hepatic and ex-proved liver LPS clearance [86% 051. The anhepatic phase in-24 h before explantation, while con-duced splanchnic ischaemia which trols (n = 8) received normal saline. correlated with portal endotoxaGastric and sigrnoid intramucosal emia. Donor preconditioning with pH (pHi), LPS and endotoxin-neu-GdCI, leads to lower systemic LPS tralising capacity (ENC) levels were concentrations in the recipient and measured in the portal vein and su-increases ENC values in the early perior vena cava after laparatomy, at phase after OLT. An improved the end of the anhepatic phase and hepatocellular LPS extraction a n d 1 h after reperfusion. During the or an activation of the extrahepatic anhepatic phase, the sigmoid pHi reticulo-endothelial system as a redecreased significantly from sult of GdC1, treatment is discussed.7.32 * 0.02 to 7.29 i 0.03 (P < 0.001) and was associated with a substan-

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