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Am J Physiol Gastrointest Liver Physiol 280: G968-G973, 2001;
0193-1857/01 $5.00
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Vol. 280, Issue 5, G968-G973, May 2001

Compensatory hepatic regeneration after mild, but not fulminant, intraperitoneal sepsis in rats

Yoram G. Weiss1,2, Lisa Bellin1, Patrick K. Kim3, Kenneth M. Andrejko1, Charlotte A. Haaxma1, Nichelle Raj1, E. Elizabeth Furth4, and Clifford S. Deutschman1,2

Departments of 1 Anesthesia, 3 Surgery, and 4 Pathology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104-4283; and 2 Department of Anesthesiology and Critical Care Medicine, Hadassah University Hospital, Jerusalem, Israel

Sepsis is the leading cause of death in surgical intensive care units. Although both mild sepsis secondary to cecal ligation and single puncture (CLP) and fulminant, double puncture CLP (2CLP) may provoke hepatocyte death, we hypothesize that regeneration compensates for cell death after CLP but not 2CLP. In male Sprague-Dawley rats, hepatic necrosis, as determined by serum alpha -glutathione S-transferase (alpha -GST) levels, was significantly but equally elevated over time after both CLP and 2CLP. Apoptosis, evaluated using both terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling and morphological examination, was minimal after both CLP and 2CLP. Regeneration, assayed by staining tissue for incorporation of exogenously administered bromodeoxyuridine, was present after CLP but not after 2CLP. To further substantiate impaired regeneration, steady-state levels of mRNAs encoding JunB, LRF-1, and cyclin D1 were determined. After 2CLP, the absence of JunB, LRF-1, and cyclin D1 mRNAs confirmed failed activation of the mitogen-activated protein kinase-linked proliferative pathway and progression through the cell cycle. Therefore, failed hepatocyte regeneration may be a manifestation of hepatic dysfunction in fulminant sepsis.

necrosis; apoptosis; liver; hepatocyte; cytokines; tumor necrosis factor; interleukin-1; interleukin-6; bromodeoxyuridine; tunel; alpha -glutathione S-transferase; cyclin D1; LRF-1; JunB


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