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: Mechanisms of gastrointestinal damage by NSAIDS.
    Author: Rainsford KD.
    Journal: Agents Actions Suppl; 1993; 44():59-64. PubMed ID: 8372736.
    Abstract:
    The multifactorial basis of gastro-intestinal (GI) damage from NSAIDs includes effects of these drugs in producing microvascular injury. Increased 5-lipoxygenase (5-LO) activity reflected in production in the gastric efferent circulation of leukotriene C-4 is shown in pigs given i.g. indomethacin. Blockade of 5-LO activity by highly selective inhibitors of this enzyme inhibits production of both gastric and intestinal leukotrienes (LT) in rats and mice. Long-term effects of NSAIDs were investigated in pigs and human volunteers. In pigs gastric ulcers occurred from oral diclofenac (Voltaren) tablets (5mg/kg/d for 10d), without significant blood loss (59Fe-RBCs) emphasizing limitations in measuring blood loss to relate this to pathology in the GI tract. Diclofenac-induced increase in leukotriene production was reversed by concurrent misoprostol, indicating that this drug could have effects other than replenishing PG (prostaglandin)-E in the mucosa. In male human volunteers given 4 NSAIDs for 7d a relation was established between reduced PG production in the antrum and ulcerogenic effects in this region but not in the fundus. These results emphasize the importance of examining mechanisms of action of NSAIDs under long-term dosage conditions to determine their variable effects.
    [Abstract] [Full Text] [Related] [New Search]