Sucralfate pp 71-82 | Cite as

Binding of Sucralfate to the Mucosal Surface

  • Gerald P. Morris


Much of the appeal of sucralfate as a subject of study for the experimental biologist lies in the numerous unknowns that surround its mode of action. The concept of a non-systemically acting agent that is therapeutically useful for the treatment of peptic ulcer and that works independently of effects on gastric acid secretion has its own fascination. As will become apparent, even the initial event following administration of this agent-the binding of sucralfate to the mucosa of the upper gastrointestinal tract-is not as straightforward as it might seem.


Mucosal Blood Flow Surface Epithelial Cell Mucus Glycoprotein Mucosal Secretion Acute Damage 
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  1. 1.
    Wallace JL, Morris GP, Beck PL, el al: Effects of sucralfate on gastric prostaglandin and leukotriene synthesis: Relationship to protective actions. Can J Physiol Pharmacol 66:666–670, 1988. Demonstrates localization of protection to areas in contact with bound sucralfate and that protection is independent of prostaglandin synthesis. This study also shows that adherent sucralfate has local effects on other mediators (leukotriene C4 and myeloperoxidase).PubMedCrossRefGoogle Scholar
  2. 2.
    Morris GP, Keenan CM, MacNaughton WK, el al: Protection of rat gastric mucosa by sucralfate. Effects of luminal stasis and inhibition of prostaglandin synthesis. Am J Med 86(suppl 6A):10–16, 1989. This paper describes the ability of sucralfate to maintain a pH gradient over the surface of the gastric mucosa at sites to which it is bound. The paper also describes the effects of sucralfate on gastric ultrastructure and shows that there is no significant damage produced by sucralfate.PubMedCrossRefGoogle Scholar
  3. 3.
    Romano M, Razandi M, Ivey KJ: Effect of sucralfate and its components on taurocholate-induced damage to rat gastric mucosal cells in tissue culture. Dig Dis Sci 35:467–476, 1990. The authors show that sucralfate adheres tightly to cultured gastric cells and protects them against sodium taurocholateinduced damage. Protection is not produced by sucrose octasulfate or aluminum hydroxide and does not depend on elevated prostaglandin synthesis or sulfhydryl compounds.PubMedCrossRefGoogle Scholar
  4. 4.
    Szabo S: The mode of action of sucralfate: The 1 × 1 × 1 mechanism of action. Scand J Gastroenterol 26(suppl 185):7–12, 1990. A brief and readable review that emphasizes the dynamic actions of sucralfate on the mucosa, which lists some of the mechanisms that could be involved in protection against different stages of damage, and that deals realistically with the barrier or “Band-Aid” theories of action.Google Scholar
  5. 5.
    Morris GP, Williamson TE, Abonyi S: The effects of sucralfate and luminal stasis on recovery of the chambered rat gastric mucosa from taurocholate-induced damage. Am J Med 91(suppl 2A):2S–14S, 1991. This paper establishes that, in an animal model, sucralfate can counteract the effects of indomethacin on the juxtamucosal pH gradient and can also accelerate repair mechanisms and thus prevent the development of otherwise inevitable damage in stomachs that have been damaged by bile salts.PubMedCrossRefGoogle Scholar
  6. 6.
    Nagashima R: Mechanisms of action of sucralfate. J Clin Gastroenterol 31(suppl 2):117–127, 1981. Comprehensive review of possible interactions of sucralfate with surfaces of both damaged and undamaged mucosae. Provides a good overview of the rationale behind various barrier hypotheses for actions of sucralfate.Google Scholar
  7. 7.
    Nakazawa S, Nagashima R, Samloff IM: Selective binding of sucralfate to gastric ulcer in man. Dig Dis Sci 26:297–300, 1981. Demonstrates, in humans, preferential binding of sucralfate to ulcerated tissue.PubMedCrossRefGoogle Scholar

Copyright information

© Plenum Press 1995

Authors and Affiliations

  • Gerald P. Morris
    • 1
  1. 1.Department of BiologyQueen’s UniversityKingstonCanada

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