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Colon Ascendens Stent Peritonitis (CASP) - a Standardized Model for Polymicrobial Abdominal Sepsis
06:45

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Metoclopramide and cellular immune functions during polymicrobial sepsis

R Oberbeck1, D Schmitz, K Wilsenack

  • 1Department of Trauma Surgery, University Hospital of Essen, Essen, Germany. reineroberbeck@hotmail.com

European Surgical Research. Europaische Chirurgische Forschung. Recherches Chirurgicales Europeennes
|March 10, 2004
PubMed

Insights

Metoclopramide (MCP) administration increased prolactin levels and modulated immune cell apoptosis and cytokine release in septic mice. However, MCP did not impact overall survival in this sepsis model.

Area of Science:

  • Immunology
  • Endocrinology
  • Pharmacology

Background:

  • Hemorrhage can impair cellular immune function.
  • Metoclopramide (MCP) has shown potential in restoring immune function post-hemorrhage by influencing prolactin release.

Purpose of the Study:

  • To investigate the effects of Metoclopramide (MCP) on immune responses and survival in a murine model of polymicrobial sepsis.
  • To assess MCP's impact on serum prolactin, cellular immunity, and mortality.

Main Methods:

  • Mice were induced with polymicrobial sepsis.
  • MCP was administered to assess its effects on serum prolactin, immune cell distribution, splenocyte proliferation, apoptosis, and cytokine release.
  • Survival was monitored for 48 hours post-sepsis induction.

Main Results:

  • MCP administration led to increased serum prolactin concentrations.
  • Splenocyte apoptosis rate increased, and cellular cytokine release was improved following MCP treatment.
  • MCP administration did not significantly affect the mortality rate of septic mice.

Conclusions:

  • Metoclopramide (MCP) modulates splenocyte apoptosis and cytokine release in a murine sepsis model.
  • The observed immunomodulatory effects of MCP may be mediated by increased endogenous prolactin release.
  • MCP did not improve survival in this specific polymicrobial sepsis model.

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