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Endotoxin tolerance protects against local hepatic ischemia/reperfusion injury in the rat

Department of General Surgery, Mannheim Medical School, University of Heidelberg, Mannheim, Germany, Clinical Research Group for Shock and Multi Organ Failure, University of Essen, Essen, Germany, emilio.dominguez{at}chir.ma.uni-heidelberg.de

Sascha Flohé

Clinical Research Group for Shock and Multi Organ Failure, University of Essen, Essen, Germany

Frank Siemers

Clinical Research Group for Shock and Multi Organ Failure, University of Essen, Essen, Germany

Michael Nau

Clinical Research Group for Shock and Multi Organ Failure, University of Essen, Essen, Germany

Markus Ackermann

Clinical Research Group for Shock and Multi Organ Failure, University of Essen, Essen, Germany

Markus Ruwe

Department of Pathology, University of Essen, Essen, Germany

Fritz Ulrich Schade

Clinical Research Group for Shock and Multi Organ Failure, University of Essen, Essen, Germany

Liver surgery and liver transplantation as well as circulatory shock are often associated with hepatic ischemia/reperfusion (I/R) injury. Recent evidence suggests that TNF- plays a central role in I/R injury and, therefore, down-regulation of TNF- seems to be a promising way to protect against the deleterious consequences of I/R. Endotoxin tolerance represents a state of unresponsiveness to endotoxin and is associated with diminished TNF- production. Thus, the effect of endotoxin tolerance on hepatic I/R injury of the liver was investigated in a rat model. I/R injury was induced by temporary ischemia of the left lateral liver lobe for 90 min followed by a 3 h observation period of reperfusion. I/R injury resulted in functional hepatic disorder characterized by a decrease both in bile flow and bile acid concentration and 50% mortality. This was prevented by induction of endotoxin tolerance. Hepatic TNF- mRNA expression after I/R of the liver was determined by RT-PCR. In untreated rats, TNF- mRNA was induced in the liver 60 min after reperfusion and further increased until 3 h after reperfusion. In contrast, in endotoxin-tolerant rats, no increases in TNF- mRNA expression were detected. This suggests that induction of endotoxin tolerance protects against hepatic I/R injury possibly via down-regulation of intra-organ TNF- expression.

Journal of Endotoxin Research, Vol. 6, No. 4, 321-328 (2000)
DOI: 10.1177/09680519000060040801


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