TY - JOUR
T1 - Influence of humoral immunoreaction on hepatic nonparenchymal cells in ex situ xenoperfused rat livers
AU - Uesugi, Takehiko
AU - Ikai, Iwao
AU - Satoh, Seiji
AU - Yagi, Toshikazu
AU - Kanazawa, Akiyoshi
AU - Takeyama, Osamu
AU - Nishitai, Ryuta
AU - Okabe, Hiroshi
AU - Katsura, Nagato
AU - Terajima, Hiroaki
AU - Takahashi, Rei
AU - Yamaoka, Yoshio
N1 - Funding Information:
1 This study was supported in part by Grants 09557105, 10044270, 10357010, and 11470244 from the Scientific Research Fund of the Ministry of Education, Science, Sports and Culture, Japan, and Grant JSPS-RFTF 96I00204 from the Research for the Future of Japan Society for the Promotion of Science.
PY - 2001
Y1 - 2001
N2 - Background. The influence of xenogeneic humoral immunoreaction on hepatic nonparenchymal cells (NPCs) was evaluated ex situ in xenoperfused rat livers. Methods. Isolated rat livers were perfused via the portal vein (PV) for 240 min. The perfusates consisted of fresh rat blood (group 1), fresh human blood (group 2), and fresh human blood containing 5 μg/mL soluble complement receptor type 1 (Group 3). Results. Deposition of human IgM and C5b-9 complement was observed in group 2, although only human IgM deposition was detected in group 3. Portal vein pressure in group 2 rose drastically during the first 10 min. Creatine kinase BB component gradually increased in all groups, followed by an elevation in alanine aminotransferase and both parameters were significantly higher in group 2 than in groups 1 and 3. In group 2, platelet thrombi in the peripheral PVs and periportal hemorrhage were observed after 10 min, and massive necrosis around the central veins after 240 rain; these changes were not observed in group 1 or 3. Production of tumor necrosis factor α and α interferon and expression of intercellular adhesion molecule 1 (ICAM-1) were lower in group 2 than in groups 1 and 3. In group 2, there were negative areas for ICAM-1 and tumor necrosis factor α staining around the central veins after 240 min, which were consistent with necrotic areas. Conclusions. In xenoperfused rat livers, humoral mediators initially caused the disturbance of microcirculation, which would induce long ischemia in the pericentral areas, resulting in massive necrosis. NPC necrosis may be responsible for less production of cytokines and adhesion molecules in the xenoperfused livers.
AB - Background. The influence of xenogeneic humoral immunoreaction on hepatic nonparenchymal cells (NPCs) was evaluated ex situ in xenoperfused rat livers. Methods. Isolated rat livers were perfused via the portal vein (PV) for 240 min. The perfusates consisted of fresh rat blood (group 1), fresh human blood (group 2), and fresh human blood containing 5 μg/mL soluble complement receptor type 1 (Group 3). Results. Deposition of human IgM and C5b-9 complement was observed in group 2, although only human IgM deposition was detected in group 3. Portal vein pressure in group 2 rose drastically during the first 10 min. Creatine kinase BB component gradually increased in all groups, followed by an elevation in alanine aminotransferase and both parameters were significantly higher in group 2 than in groups 1 and 3. In group 2, platelet thrombi in the peripheral PVs and periportal hemorrhage were observed after 10 min, and massive necrosis around the central veins after 240 rain; these changes were not observed in group 1 or 3. Production of tumor necrosis factor α and α interferon and expression of intercellular adhesion molecule 1 (ICAM-1) were lower in group 2 than in groups 1 and 3. In group 2, there were negative areas for ICAM-1 and tumor necrosis factor α staining around the central veins after 240 min, which were consistent with necrotic areas. Conclusions. In xenoperfused rat livers, humoral mediators initially caused the disturbance of microcirculation, which would induce long ischemia in the pericentral areas, resulting in massive necrosis. NPC necrosis may be responsible for less production of cytokines and adhesion molecules in the xenoperfused livers.
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U2 - 10.1006/jsre.2001.6182
DO - 10.1006/jsre.2001.6182
M3 - Article
C2 - 11469897
AN - SCOPUS:0034899493
SN - 0022-4804
VL - 99
SP - 272
EP - 281
JO - Journal of Surgical Research
JF - Journal of Surgical Research
IS - 2
ER -