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: [Suppression of hypotalamic-pituitary-adrenocortical system as a reason of aggravation of indomethacin-induced gastric ulcerogenic effect by cortisol treatment with pharmacological dose].
    Author: Morozova OIu, Bagaeva TR, Filaretova LP.
    Journal: Ross Fiziol Zh Im I M Sechenova; 2008 Nov; 94(11):1291-9. PubMed ID: 19140306.
    Abstract:
    In the present study, we verified the hypothesis that an aggravated effect of glucocorticoid therapy on indomethacin-induced gastric erosion formation could be due to a deficiency of glucocorticoid production caused by suppression of the hypothalamic-pituitary-adrenocortical system (HPAS). Gastric erosions were induced by indomethacin (25 mg/kg, sc) in rats after 24 h fasting. The effects of cortisol pharmacological dose on indomethacin-induced gastric erosions and plasma corticosterone levels were investigated 1 and 4 weeks after cortisol pretreatment. Indomethacin caused a plasma corticosterone rise that was almost fully prevented in cortisol-pretreated rats 1 week after the pretreatment. Indomethacin-induced gastric erosions were significantly aggravated 1 week after cortisol pretreatment, and an acute corticosterone replacement mimicking indomethacin-induced corticosterone rise prevented this aggravation. 4 weeks after cortisol pretreatment, both corticosterone and gastric responses to indomethacin were restored. The results suggest that suppression HPAS function seems to be a reason of an aggravated effect of glucocorticoid therapy on indomethacin-induced gastric erosions.
    [Abstract] [Full Text] [Related] [New Search]