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Nitrergic modulation of gastrointestinal function during early endotoxemia.

E Quintana1, M D Barrachina, J V Esplugues

  • 1Department of Pharmacology, Faculty of Medicine, University of Valencia, Avd. Blasco Ibáñez 15, 46010 Valencia, Spain.

Current Pharmaceutical Design
|December 16, 2006
PubMed
Summary

Bacterial infections trigger an acute phase response affecting gastrointestinal function. Early endotoxemia involves nitric oxide (NO) synthesis via constitutive nitric oxide synthase (NOS) in the nervous system, influencing gut changes.

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Area of Science:

  • Gastroenterology
  • Neuroscience
  • Immunology

Background:

  • Bacterial infections initiate an acute phase response involving physiological, neuroendocrine, and behavioral changes.
  • Endotoxemia, particularly from Gram-negative bacteria, causes fever, appetite loss, and altered gastrointestinal function to restore homeostasis.
  • Nitric oxide (NO) is crucial for gastrointestinal physiology and its response to illness.

Purpose of the Study:

  • To review experimental evidence supporting the role of physiological mechanisms in acute gastrointestinal changes during early endotoxemia.
  • To investigate the involvement of the autonomic and central nervous systems in these early endotoxemia-induced gut responses.
  • To explore the contribution of constitutive nitric oxide synthase (NOS) isoforms to rapid gastrointestinal alterations.

Main Methods:

  • Systemic administration of low-dose endotoxin (5-40 microg/kg) to rats.
  • Observation of rapid onset changes in gastrointestinal motor function, gastric acid secretion, and mucosal resistance.
  • Measurement of nitric oxide (NO) synthesis in the brainstem and gastric myenteric plexus.

Main Results:

  • Low-dose endotoxin administration rapidly alters rat gastrointestinal motor function, inhibits gastric acid secretion, and increases mucosal resistance.
  • These rapid changes are not linked to vascular dysfunction and involve both peripheral and central nervous systems.
  • Increased NO synthesis, mediated by constitutive NOS, occurs in the brainstem and gastric myenteric plexus within 30 minutes of endotoxin administration, preceding NOS induction.

Conclusions:

  • Early endotoxemia-induced gastrointestinal changes are mediated by a physiological mechanism involving the autonomic and central nervous systems.
  • Constitutive nitric oxide synthase (NOS) isoforms play a key role in the rapid onset of these gastrointestinal alterations.
  • Understanding these mechanisms is vital for managing the gastrointestinal complications of bacterial infections.