PMID- 7487464
OWN - NLM
STAT- MEDLINE
DCOM- 19951205
LR  - 20190704
IS  - 0004-0010 (Print)
IS  - 0004-0010 (Linking)
VI  - 130
IP  - 11
DP  - 1995 Nov
TI  - The possible role of a central nervous system dopaminergic mechanism in hepatic 
      c-fos protein expression following peritoneal sepsis.
PG  - 1209-15; discussion 1215-6
AB  - OBJECTIVE: To investigate the hypothesis that a central dopaminergic mechanism 
      may regulate hepatic c-fos and c-jun gene expression following peritoneal sepsis. 
      METHODS: First, dopamine or vehicle was instilled into a stereotaxically placed 
      intracerebral-ventricular (ICV) cannula with or without D1 (SCH 23390) or D2 
      (haloperidol) antagonist pretreatment in a rat model, and the effect on hepatic 
      c-fos or c-jun protein expression was investigated. Second, we investigated the 
      effect of haloperidol and vehicle treatment following cecal ligation and puncture 
      (CLP)-induced sepsis with respect to hepatic c-fos protein expression, c-jun 
      protein expression, and survival. RESULTS: Intracerebral-ventricular dopamine 
      treatment increased hepatic c-fos immunoreactive protein but had no effect on 
      hepatic c-jun immunoreactive protein expression. Pretreatment with SCH 23390 
      inhibited ICV dopamine treatment-induced hepatic c-fos immunoreactive protein 
      expression. Haloperidol pretreatment synergized with ICV dopamine treatment to 
      overexpress hepatic c-fos protein. Haloperidol treatment significantly increased 
      CLP-induced hepatic c-fos and c-jun protein expression and improved survival 
      following CLP. CONCLUSIONS: Hepatic c-fos protein expression may be regulated, in 
      part, by a central nervous system-mediated dopaminergic D1 receptor mechanism. 
      Treatment with the D2 receptor antagonist, haloperidol, increases sepsis-induced 
      hepatic c-fos and c-jun protein expression and improves survival following 
      peritoneal contamination.
FAU - Roy, S
AU  - Roy S
AD  - Department of Surgery, University of Minnesota, Minneapolis, USA.
FAU - Charboneau, R
AU  - Charboneau R
FAU - Cain, K J
AU  - Cain KJ
FAU - Chapin, R B
AU  - Chapin RB
FAU - Barke, R A
AU  - Barke RA
LA  - eng
GR  - DA 08188/DA/NIDA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Arch Surg
JT  - Archives of surgery (Chicago, Ill. : 1960)
JID - 9716528
RN  - 0 (Dopamine Antagonists)
RN  - 0 (Receptors, Dopamine)
RN  - VTD58H1Z2X (Dopamine)
SB  - IM
MH  - Animals
MH  - Brain/physiology
MH  - Dopamine/*physiology
MH  - Dopamine Antagonists/pharmacology
MH  - Genes, fos/*genetics
MH  - Genes, jun/*genetics
MH  - Liver/*metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, Dopamine/*physiology
MH  - Sepsis/*metabolism
EDAT- 1995/11/01 00:00
MHDA- 1995/11/01 00:01
CRDT- 1995/11/01 00:00
PHST- 1995/11/01 00:00 [pubmed]
PHST- 1995/11/01 00:01 [medline]
PHST- 1995/11/01 00:00 [entrez]
AID - 10.1001/archsurg.1995.01430110067012 [doi]
PST - ppublish
SO  - Arch Surg. 1995 Nov;130(11):1209-15; discussion 1215-6. doi: 
      10.1001/archsurg.1995.01430110067012.