PMID- 12477079
OWN - NLM
STAT- MEDLINE
DCOM- 20030507
LR  - 20191106
IS  - 1023-3830 (Print)
IS  - 1023-3830 (Linking)
VI  - 51
IP  - 10
DP  - 2002 Oct
TI  - Endotoxin tolerance in rats: influence on LPS-induced changes in excretory liver 
      function.
PG  - 500-5
AB  - OBJECTIVE AND DESIGN: We investigated in a rat model of endotoxic shock whether 
      endotoxin tolerance (ETT) prevents lipopolysaccharide (LPS) associated lethality 
      and studied the initial function of liver response to LPS. ANIMALS: Male 
      Sprague-Dawley rats. TREATMENT: ETT was induced by i.p. injection of LPS 
      (Salmonella friedenau) intraperitoneally over 5 days. Rats (n = 6 each group) 
      received 1 mg LPS/kg b. w. intravenously (Salmonella friedenau). The common bile 
      duct was then canalized and bile was collected every 60 min for 6 h. 1 h after 
      LPS-application liver biopsies were taken for determination of TNF-alpha by 
      RT-PCR. Sham operated animals (n = 6 each group) were treated identically but 
      without application of LPS. RESULTS: All ETT animals survived the duration of the 
      experiment whereas non-tolerant animals (NETT) died before the end of the 
      experiment (5/6). NETT animals showed a continuous decrease in bile flow after 
      240 min. The amount of bile acids was significantly lower (ANOVA) in NETT animals 
      than in sham operated controls or ETT-animals. Analysis of TNF-alpha mRNA 
      expression in the liver revealed an upregulation 1 h after LPS application, which 
      was significantly lower in LPS-tolerant animals. CONCLUSIONS: Our results show 
      that excretory liver failure and death subsequent to intravenous LPS application 
      can be successfully counteracted by induction of ETT.
FAU - Dominguez Fernandez, E
AU  - Dominguez Fernandez E
AD  - Department of General Surgery, Mannheim Medical School, University of Heidelberg, 
      Theodor Kutzer-Ufer 1-3, DE-68167 Mannheim, Germany. 
      emilio.dominguez@chir.ma.uni-heidelberg.de
FAU - Flohe, S
AU  - Flohe S
FAU - Siemers, F
AU  - Siemers F
FAU - Nau, M
AU  - Nau M
FAU - Schade, F U
AU  - Schade FU
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Switzerland
TA  - Inflamm Res
JT  - Inflammation research : official journal of the European Histamine Research 
      Society ... [et al.]
JID - 9508160
RN  - 0 (Bile Acids and Salts)
RN  - 0 (DNA, Complementary)
RN  - 0 (Endotoxins)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 63231-63-0 (RNA)
SB  - IM
MH  - Animals
MH  - Bile/physiology
MH  - Bile Acids and Salts/metabolism
MH  - DNA, Complementary/biosynthesis
MH  - Drug Tolerance
MH  - Endotoxins/*toxicity
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Lipopolysaccharides/*toxicity
MH  - Liver/drug effects/*metabolism/pathology
MH  - Male
MH  - RNA/biosynthesis/isolation & purification
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Salmonella/chemistry
MH  - Tumor Necrosis Factor-alpha/metabolism
EDAT- 2002/12/13 04:00
MHDA- 2003/05/08 05:00
CRDT- 2002/12/13 04:00
PHST- 2002/12/13 04:00 [pubmed]
PHST- 2003/05/08 05:00 [medline]
PHST- 2002/12/13 04:00 [entrez]
AID - 10.1007/pl00012419 [doi]
PST - ppublish
SO  - Inflamm Res. 2002 Oct;51(10):500-5. doi: 10.1007/pl00012419.