These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Experimental stress ulcers: a review.
    Author: Butterfield WC.
    Journal: Surg Annu; 1975; 7():261-78. PubMed ID: 1101403.
    Abstract:
    The restraint model and other models for the production of experimental stress ulcers have been reviewed. The mechanism of experimental stress ulcers appears to depend on an interaction between the presence of acid, changes in mucosal circulation, an increase in the excretion of glycoproteins in the mucus, and a decrease in mitotic activity of the mucosal lining of the stomach. Factors enhancing ulceration are cold, starvation, increased acidity, burns, reflux of bile, endotoxin, adrenalectomy, and hemorrhage. Factors inhibiting ulceration are vagotomy, anticholinergics, elemental diets, vitamin A, antacids, prevention of bile reflux, corticosteroids, epinephrine and norepinephrine, serotonin antagonists, and immediate replacement of blood loss with low molecular weight dextran. The role of sepsis is unclear and more work is needed in this area. Ulcers from intracranial injury are usually associated with the hypersecretion of gastric acid. Stimulation of the hypothalamus, directly or indirectly, with resultant vagal stimulation is thought to be the responsible mechanism for the increase in acid.
    [Abstract] [Full Text] [Related] [New Search]