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Article |

The Possible Role of a Central Nervous System Dopaminergic Mechanism in Hepatic c-fos Protein Expression Following Peritoneal Sepsis

Sabita Roy, PhD; Richard Charboneau; Kelly J. Cain, MS; Rebecca B. Chapin, PhD; Roderick A. Barke, MD
Arch Surg. 1995;130(11):1209-1216. doi:10.1001/archsurg.1995.01430110067012.
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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 immunore-active 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.(Arch Surg. 1995;130:1209-1216)


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