Discrimination of site-specific alterations in gastrointestinal permeability in the rat

Gastroenterology. 1998 Jan;114(1):83-92. doi: 10.1016/s0016-5085(98)70636-5.


Background & aims: Detection of gastrointestinal damage can be accomplished by permeability testing. However, current methodology presents several problems, including lack of site specificity and an inability to easily measure colonic damage. We hypothesized that probes of similar size could be used to simultaneously assess permeability along the length of the gastrointestinal tract. Differentiation of damage sites could be made, provided that probes were selectively destroyed at different levels. Class 1 probes should be destroyed after leaving the stomach, class 2 after leaving the small intestine, and class 3 not at all. In this manner, class 1 probes would report damage to the proximal gut, class 2 to the small intestine, and class 3 to the gut as a whole.

Methods: We defined saccharide probes with these characteristics and observed their permeability patterns in defined models of localized gastrointestinal damage.

Results: With gastric damage, permeability of only class 1 probes increased, whereas with colonic damage only permeation rates of class 3 probes was increased. Furthermore, the permeation rates of both class 2 and 3 probes increased in the presence of small intestinal disease.

Conclusions: These techniques allow a single screening test that is sensitive to damage at any level of the gastrointestinal tract and may be used in either animals or humans.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Aspirin / metabolism
  • Aspirin / toxicity
  • Biological Transport
  • Cyclooxygenase Inhibitors / metabolism
  • Cyclooxygenase Inhibitors / toxicity
  • Digestive System / drug effects
  • Digestive System / metabolism
  • Digestive System / pathology*
  • Disease Models, Animal
  • Gastrointestinal Diseases / pathology*
  • Indomethacin / metabolism
  • Indomethacin / toxicity
  • Rats
  • Trinitrobenzenesulfonic Acid / metabolism
  • Trinitrobenzenesulfonic Acid / toxicity


  • Cyclooxygenase Inhibitors
  • Trinitrobenzenesulfonic Acid
  • Aspirin
  • Indomethacin