The mechanism of aggravation of indomethacin-induced gastric ulcers by adrenalectomy in the rat.

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  • URUSHIDANI Tetsuro
    Department of Chemical Pharmacology, Faculty of Pharmaceutical Sciences, University of Tokyo
  • KASUYA Yutaka
    Department of Chemical Pharmacology, Faculty of Pharmaceutical Sciences, University of Tokyo
  • OKABE Susumu
    Department of Applied Pharmacology, Kyoto College of Pharmacy

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  • Mechanism of Aggravation of Indomethaci

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Bilateral adrenalectomy markedly aggravated gastric ulcers in rats induced by 5 or 20 mg/kg of indomethacin. The degree of aggravation was much the same in experiments done 1 and 14 days after operation. Pretreatment with prednisolone 10 mg/kg or cortisone acetate 10 mg/kg given subcutaneously significantly suppressed the aggravated ulceration in response to 20 mg/kg of indomethacin in these adrenalectomized rats. Desoxycorticosterone acetate 10 mg/kg, however, had no effect on the aggravation of indomethacin-induced ulcers. Epinephrine 0.1 or 1 mg/kg given subcutaneously markedly suppressed the indomethacin-induced ulcers in adrenalectomized rats. Removal of the adrenal medulla alone did not appreciably influence the development of indomethacin-induced ulcers. These results indicate that the adrenal cortex, particularly the area containing glucocorticoids, plays an important role in suppression of the noxious effect of indomethacin on the rat gastric mucosa.

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