Digestive Diseases and Sciences

, Volume 35, Issue 8, pp 984–992 | Cite as

Possible mechanisms involved in gastric hypermotility caused by indomethacin in the rat

Role of glycoprivic response
  • Koji Takeuchi
  • Megumu Okada
  • Hiromichi Niida
  • Susumu Okabe
Original Articles

Abstract

Pathogenesis of indomethacin-induced gastric lesions was investigated in the rat by measuring lesions, gastric motility, and terminal blood glucose levels and correlating them with each other. Subcutaneously administered indomethacin (3–25 mg/kg) dose-dependently produced lesions in the stomach with concomitant gastric hypermotility and reduction of blood glucose levels. When the lesion score and the motility were plotted against terminal glucose levels, a highly significant relationship was found among these three factors (P < 0.01). Gastric lesions and hypermotility induced by indomethacin (25 mg/kg) were suppressed significantly by 16,16-dmPGE2 (10 Μg/kg) with no effect on the glucose levels, while intravenous infusion of glucose (25% w/w, 1.4 ml/hr) prevented these responses and restored the reduced glucose levels above the basal values. In addition, both 16,16-dmPGE2 and glucose infusion afforded a significant protection against gastric lesions induced by indomethacin even in the acid-perfused stomach (150 mM HCl). These results confirmed gastric hypermotility as a key element in the pathogenesis of indomethacin-induced lesions and further suggested that indomethacin may sensitize gastric contractility through glycoprivic receptors by inducing hypoglycemia and PG deficiency.

Key words

indomethacin gastric lesion gastric motility blood glucose glycoprivic response 

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Copyright information

© Plenum Publishing Corporation 1990

Authors and Affiliations

  • Koji Takeuchi
    • 1
  • Megumu Okada
    • 1
  • Hiromichi Niida
    • 1
  • Susumu Okabe
    • 1
  1. 1.Department of Applied PharmacologyKyoto Pharmaceutical UniversityKyotoJapan

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