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Ischemia of rat stomach mobilizes ECL cell histamine

In English

Författare

  • M Kitano
  • Maria Lundgren
  • Y Kishimoto
  • Per Norlén
  • Rolf Håkanson
  • Y Haenuki
  • M Kudo
  • J Hasegawa

Summary, in English

Microdialysis was used to study how ischemia-evoked gastric mucosal injury affects rat stomach histamine, which resides in enterochromaffin-like (ECL) cells and mast cells. A microdialysis probe was inserted into the gastric submucosa, and the celiac artery was clamped (30 min), followed by removal of the clamp. Microdialysate histamine was determined by enzyme-linked immunosorbent assay. In addition, we studied the long-term effects of ischemia on the oxyntic mucosal histidine decarboxylase activity in omeprazole-treated rats. Gastric mucosal lesions induced by the ischemia were enlarged on removal of the clamp. The microdialysate histamine concentration increased immediately on clamping (50-fold rise within 30 min) and declined promptly after the clamp was removed. In contrast, histidine decarboxylase activity of the ECL cells was lowered by the ischemia and returned to preischemic values 9 days later. Mast cell-deficient rats responded to ischemia-reperfusion much like wild-type rats with respect to histamine mobilization. Pretreatment with the irreversible inhibitor of histidine decarboxylase, alpha-fluoromethylhistidine, which is known to eliminate histamine from ECL cells, prevented the rise in microdialysate histamine. Pharmacological blockade of acid secretion (cimetidine or omeprazole) prevented the lesions induced by ischemia-reperfusion insult but not the mobilization of histamine. In conclusion, ischemia of the celiac artery mobilizes large amounts of histamine from ECL cells, which occurs independently of the gross mucosal lesions. The prompt reduction of the mucosal histidine decarboxylase activity in response to ischemia probably reflects ECL cell damage. The lesions develop not because of mobilization of histamine per se but because of ischemia plus reperfusion plus gastric acid.

Publiceringsår

2005

Språk

Engelska

Sidor

1084-1090

Publikation/Tidskrift/Serie

American Journal of Physiology: Gastrointestinal and Liver Physiology

Volym

288

Issue

5

Dokumenttyp

Artikel i tidskrift

Förlag

American Physiological Society

Ämne

  • Physiology

Nyckelord

  • enterochromaffin-like cell
  • ischemia-reperfusion
  • histidine
  • decarboxylase

Status

Published

Forskningsgrupp

  • Drug Target Discovery

ISBN/ISSN/Övrigt

  • ISSN: 1522-1547