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Indomethacin‐induced gastric antral damage in hamsters: are neutrophils involved?
Author(s) -
| Fitzpatrick,
Sakurai,
; Le
Publication year - 1999
Publication title -
alimentary pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.308
H-Index - 177
eISSN - 1365-2036
pISSN - 0269-2813
DOI - 10.1046/j.1365-2036.1999.00444.x
Subject(s) - medicine , antrum , myeloperoxidase , pathophysiology , hamster , stomach , gastroenterology , gastric mucosa , cheek pouch , pathology , inflammation
Background: A direct role for neutrophils in the pathophysiology of indomethacin‐induced gastric damage is controversial. Therefore, such damage was evaluated in hamsters. Methods: Gastric antral damage was evaluated 4 h after the oro‐gastric administration of indomethacin (30 mg/kg). Prior to indomethacin, hamsters were treated with various pharmacological agents: rebamipide, methotrexate or anti‐neutrophil serum (ANS). The number of circulating neutrophils was determined from Wright–Giemsa stained blood smears. Myeloperoxidase (MPO) activity was measured as a marker of gastric antral neutrophil infiltration. Results: Indomethacin caused primarily gastric antral damage. By histology, this damage did not penetrate the muscularis mucosa. A significant increase in gastric antral MPO activity was also found in indomethacin‐treated hamsters. Rebamipide decreased macroscopic gastric antral damage in a dose‐related fashion. Methotrexate treatment reduced the circulating blood neutrophil number by 38–44%, but did not affect gastric damage. ANS treatment resulted in near complete neutropenia, and also in a substantial reduction (84%) in gastric antral MPO activity. However, gastric antral damage was not significantly altered by ANS. Conclusions: Neutrophils are not directly involved in the pathophysiology of indomethacin‐induced damage to the hamster gastric antrum.