An Experimental Study on Damage of Hepatic Regeneration due to Bile Peritonitis after Partial Hepatectomy -Lipid Peroxidation of Liver Remnant-

Kenji Fukuhara, Kiyoaki Ouchi, Seiki Matsuno

The First Department of Surgery, Tohoku University School of Medicine

Experimental studies were performed to clarify why bile peritonitis after partial hepatectomy inhibits hepatic regeneration. Rats underwent 70% hepatectomy (Hx group), bile peritonitis after Hx (Hx+P group), and Hx+P with administration of catalase and recombinant human SOD (S group). The labelling indexes at 24 and 48 hours after hepatectomy were 22.4% and 7.5% in the Hx group, 4.4 and 8.8% in the Hx+P group, and 6.4 and 24.5% in the S group, respectively. An initiation of DNA synthesis delayed and a peak level of it diminished in the Hx+P group, but the former improved in the S group. Lipoperoxide (LPO) of the liver remnant did not increase in the Hx group throughout 48 hours after hepatectomy. In contrast, LPO in the Hx+P group showed significant, continuous elevation from 12 hours after hepatectomy. In the S group, however, LPO was reduced to almost half that in the Hx+P group. The energy charge of the liver remnant in the Hx+P group was significantly lower than that in the Hx group, and systemic endotoxin levels were high only in the Hx+P group. In conclusion, bile peritonitis after partial hepatectomy induced delayed initiation and a diminished peak level of DNA synthesis. Although an elevated level of endotoxin may play a partial role in increased lipid peroxidation, accumulated bile components may cause acceleration of lipid peroxidation and inhibited hepatic regeneration because of mitochondrial membrane damage.

Key words
bile peritonitis, hepatic regeneration, hepatectomy, lipid peroxidation, scavenger

Reprint requests
Kenji Fukuhara The First Department of Surgery, Tohoku University School of Medicine
1-1 Seiryou-machi, Aoba-ku, Sendai, 980 JAPAN

Accepted
November 1, 1993

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