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Ischemia of rat stomach mobilizes ECL cell histamine

Kitano, M; Lundgren, Maria LU ; Kishimoto, Y; Norlén, Per LU ; Håkanson, Rolf LU ; Haenuki, Y; Kudo, M and Hasegawa, J (2005) In American Journal of Physiology: Gastrointestinal and Liver Physiology 288(5). p.1084-1090
Abstract
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... (More)
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. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
enterochromaffin-like cell, ischemia-reperfusion, histidine, decarboxylase
in
American Journal of Physiology: Gastrointestinal and Liver Physiology
volume
288
issue
5
pages
1084 - 1090
publisher
American Physiological Society
external identifiers
  • pmid:15662050
  • wos:000228282500030
  • scopus:17644382290
ISSN
1522-1547
DOI
10.1152/ajpgi.00004.2004
language
English
LU publication?
yes
id
6853cc4c-8432-45d5-84da-7216b2081b6b (old id 246580)
date added to LUP
2007-08-15 11:44:19
date last changed
2017-05-21 03:30:08
@article{6853cc4c-8432-45d5-84da-7216b2081b6b,
  abstract     = {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.},
  author       = {Kitano, M and Lundgren, Maria and Kishimoto, Y and Norlén, Per and Håkanson, Rolf and Haenuki, Y and Kudo, M and Hasegawa, J},
  issn         = {1522-1547},
  keyword      = {enterochromaffin-like cell,ischemia-reperfusion,histidine,decarboxylase},
  language     = {eng},
  number       = {5},
  pages        = {1084--1090},
  publisher    = {American Physiological Society},
  series       = {American Journal of Physiology: Gastrointestinal and Liver Physiology},
  title        = {Ischemia of rat stomach mobilizes ECL cell histamine},
  url          = {http://dx.doi.org/10.1152/ajpgi.00004.2004},
  volume       = {288},
  year         = {2005},
}