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Related Experiment Videos

Increased gut permeability following burn trauma.

M D Epstein1, J I Tchervenkov, J W Alexander

  • 1Department of Surgery, University of Cincinnati Medical Center, Shriners Burns Institute, Ohio.

Archives of Surgery (Chicago, Ill. : 1960)
|February 1, 1991
PubMed
Summary

Burn injury significantly increases gut permeability to lactulose, a paracellular marker, especially within 48 hours. Permeability to L-rhamnose, a transcellular marker, remained unchanged, indicating a paracellular mechanism of gut barrier dysfunction post-burn.

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Area of Science:

  • Physiology
  • Surgical Research
  • Gastroenterology

Background:

  • Burn injuries cause significant physiological stress.
  • Gastrointestinal (GI) dysfunction is a common complication after severe burns.
  • Understanding the mechanisms of GI permeability changes is crucial for patient management.

Purpose of the Study:

  • To investigate the impact of burn injury on gastrointestinal permeability in a guinea pig model.
  • To differentiate between paracellular and transcellular routes of absorption changes post-burn.
  • To determine the temporal profile of GI permeability alterations after burn trauma.

Main Methods:

  • Twenty female Hartley guinea pigs underwent a 30% full-thickness burn.
  • Gastrointestinal permeability was assessed using lactulose and L-rhamnose urinary excretion.

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  • Measurements were taken before burn and on postburn days 1, 2, 3, 7, and 14.

    • Main Results:

    • Gut permeability to L-rhamnose (transcellular marker) showed no significant increase post-burn.
    • Gut permeability to lactulose (paracellular marker) significantly increased after burn injury.
    • The greatest increase in lactulose permeability occurred within the first 48 hours post-burn.

    Conclusions:

    • Burn trauma leads to immediate increases in gut permeability, primarily via the paracellular pathway.
    • This suggests a disruption of the tight junctions between intestinal epithelial cells.
    • The findings highlight the paracellular route as a key mechanism in burn-induced GI barrier dysfunction.