Acute gastric lesions induced by the administration of histamine to rats with partial vascular occlusion: evidence for the gastroprotective effect of prostaglandin

Introduction Histamine is not only a potent stimulator of gastric acid secretion, but it also plays a central role in gastroduodenal ulcerogenesis. In the present study we tested the effect of pre-treatment with exogenous prostaglandin E₂ (PGE₂) in a new rat model of experimental gastric ulcers indu...

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Veröffentlicht in:Inflammation research 2010-03, Vol.59 (2), p.239-241
Hauptverfasser: Konturek, P. C, Brzozowski, T, Raithel, M, Sliwowski, Z, Konturek, S. J, Neurath, M. F
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container_issue 2
container_start_page 239
container_title Inflammation research
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creator Konturek, P. C
Brzozowski, T
Raithel, M
Sliwowski, Z
Konturek, S. J
Neurath, M. F
description Introduction Histamine is not only a potent stimulator of gastric acid secretion, but it also plays a central role in gastroduodenal ulcerogenesis. In the present study we tested the effect of pre-treatment with exogenous prostaglandin E₂ (PGE₂) in a new rat model of experimental gastric ulcers induced by combination of histamine and gastric ischemia. Methods In male Wistar rats, a chronic ischemia of gastric mucosa was induced via the clamping of the left gastric artery and vein (L-AV) in combination with pylorus ligation. The following treatment groups of rats (6 rats/group) were investigated: 1) histamine alone (40 mg/kg twice s.c.); 2) vehicle (saline) followed 30 min later by gastric mucosal L-AV ischemia and pylorus ligation combined with histamine (40 mg/kg twice s.c.) and 3) PGE₂ (5 µg/kg i.g.) followed 30 min later by gastric mucosal L-AV ischemia combined with histamine (40 mg/kg twice s.c.) and pylorus ligation. At 4 hr after the clamping of L-AV and pylorus ligation, the area of gastric lesions and gastric acid secretion was determined. Results Histamine treatment failed to produce gastric lesions, but when it was combined with ischemia, the widespread gastric lesions in the corpus mucosa, but not in the antrum, were observed. This damaging effect and decrease in the GBF were significantly attenuated by pretreatment with PGE₂. Conclusion The present study demonstrates that gastric hypersecretion induced by histamine in combination with gastric mucosal ischemia results in gastric lesions which progress into chronic gastric ulcers.
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C ; Brzozowski, T ; Raithel, M ; Sliwowski, Z ; Konturek, S. J ; Neurath, M. F</creator><creatorcontrib>Konturek, P. C ; Brzozowski, T ; Raithel, M ; Sliwowski, Z ; Konturek, S. J ; Neurath, M. F</creatorcontrib><description>Introduction Histamine is not only a potent stimulator of gastric acid secretion, but it also plays a central role in gastroduodenal ulcerogenesis. In the present study we tested the effect of pre-treatment with exogenous prostaglandin E₂ (PGE₂) in a new rat model of experimental gastric ulcers induced by combination of histamine and gastric ischemia. Methods In male Wistar rats, a chronic ischemia of gastric mucosa was induced via the clamping of the left gastric artery and vein (L-AV) in combination with pylorus ligation. The following treatment groups of rats (6 rats/group) were investigated: 1) histamine alone (40 mg/kg twice s.c.); 2) vehicle (saline) followed 30 min later by gastric mucosal L-AV ischemia and pylorus ligation combined with histamine (40 mg/kg twice s.c.) and 3) PGE₂ (5 µg/kg i.g.) followed 30 min later by gastric mucosal L-AV ischemia combined with histamine (40 mg/kg twice s.c.) and pylorus ligation. At 4 hr after the clamping of L-AV and pylorus ligation, the area of gastric lesions and gastric acid secretion was determined. Results Histamine treatment failed to produce gastric lesions, but when it was combined with ischemia, the widespread gastric lesions in the corpus mucosa, but not in the antrum, were observed. This damaging effect and decrease in the GBF were significantly attenuated by pretreatment with PGE₂. Conclusion The present study demonstrates that gastric hypersecretion induced by histamine in combination with gastric mucosal ischemia results in gastric lesions which progress into chronic gastric ulcers.</description><identifier>ISSN: 1023-3830</identifier><identifier>EISSN: 1420-908X</identifier><identifier>DOI: 10.1007/s00011-009-0140-5</identifier><identifier>PMID: 20020314</identifier><language>eng</language><publisher>Basel: Basel : SP Birkhäuser Verlag Basel</publisher><subject>Allergology ; Animals ; Anti-Ulcer Agents ; Biomedical and Life Sciences ; Biomedicine ; Dermatology ; Dinoprostone - pharmacology ; Disease Models, Animal ; Histamine ; Immunology ; ischemia ; Ischemia - pathology ; Ligation ; Male ; Neurology ; Pharmacology/Toxicology ; Rats ; Rats, Wistar ; Regional Blood Flow - physiology ; Rheumatology ; Short Communication ; Stomach - blood supply ; Stomach Ulcer - chemically induced ; Stomach Ulcer - pathology ; Stomach Ulcer - prevention &amp; control ; Ulcer</subject><ispartof>Inflammation research, 2010-03, Vol.59 (2), p.239-241</ispartof><rights>Birkhäuser Verlag, Basel/Switzerland 2009</rights><rights>Springer Basel AG 2010</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c346t-127e6458fc85324b70d72a86d885b2ffbd6696a158510bf6dba75e7c33b9e61b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00011-009-0140-5$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00011-009-0140-5$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>315,781,785,27929,27930,41493,42562,51324</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20020314$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Konturek, P. 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Methods In male Wistar rats, a chronic ischemia of gastric mucosa was induced via the clamping of the left gastric artery and vein (L-AV) in combination with pylorus ligation. The following treatment groups of rats (6 rats/group) were investigated: 1) histamine alone (40 mg/kg twice s.c.); 2) vehicle (saline) followed 30 min later by gastric mucosal L-AV ischemia and pylorus ligation combined with histamine (40 mg/kg twice s.c.) and 3) PGE₂ (5 µg/kg i.g.) followed 30 min later by gastric mucosal L-AV ischemia combined with histamine (40 mg/kg twice s.c.) and pylorus ligation. At 4 hr after the clamping of L-AV and pylorus ligation, the area of gastric lesions and gastric acid secretion was determined. Results Histamine treatment failed to produce gastric lesions, but when it was combined with ischemia, the widespread gastric lesions in the corpus mucosa, but not in the antrum, were observed. 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Results Histamine treatment failed to produce gastric lesions, but when it was combined with ischemia, the widespread gastric lesions in the corpus mucosa, but not in the antrum, were observed. This damaging effect and decrease in the GBF were significantly attenuated by pretreatment with PGE₂. Conclusion The present study demonstrates that gastric hypersecretion induced by histamine in combination with gastric mucosal ischemia results in gastric lesions which progress into chronic gastric ulcers.</abstract><cop>Basel</cop><pub>Basel : SP Birkhäuser Verlag Basel</pub><pmid>20020314</pmid><doi>10.1007/s00011-009-0140-5</doi><tpages>3</tpages></addata></record>
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subjects Allergology
Animals
Anti-Ulcer Agents
Biomedical and Life Sciences
Biomedicine
Dermatology
Dinoprostone - pharmacology
Disease Models, Animal
Histamine
Immunology
ischemia
Ischemia - pathology
Ligation
Male
Neurology
Pharmacology/Toxicology
Rats
Rats, Wistar
Regional Blood Flow - physiology
Rheumatology
Short Communication
Stomach - blood supply
Stomach Ulcer - chemically induced
Stomach Ulcer - pathology
Stomach Ulcer - prevention & control
Ulcer
title Acute gastric lesions induced by the administration of histamine to rats with partial vascular occlusion: evidence for the gastroprotective effect of prostaglandin
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