| dc.contributor.author | Gidener C. | |
| dc.contributor.author | Rizalar R. | |
| dc.contributor.author | Baris S. | |
| dc.contributor.author | Bernay R. | |
| dc.contributor.author | Gurses N. | |
| dc.date.accessioned | 2020-06-21T09:19:50Z | |
| dc.date.available | 2020-06-21T09:19:50Z | |
| dc.date.issued | 1995 | |
| dc.identifier.issn | 1300-0144 | |
| dc.identifier.uri | https://hdl.handle.net/20.500.12712/3158 | |
| dc.description.abstract | Stress ulcers are acute gastric mucosal lesions developing as a result of the mucosal ischemia due to several initiating factors. It has been shown that the majority of tissue injury occurs during the reperfusion period when the oxygen derived free radicals, form and meet tissue. We have used an animal model to investigate the intensity and mechanism of tissue injury in stress ulceration with or without reperfusion. The role of oxygen radicals were also investigated. We have shown that the intensity of tissue injury is greatest in the reperfused group and that further injury can be prevented by deferoxamine which inhibits the formation of hydroxyl radicals. | en_US |
| dc.language.iso | eng | en_US |
| dc.rights | info:eu-repo/semantics/closedAccess | en_US |
| dc.subject | deferoxamine | en_US |
| dc.subject | ischemia/reperfusion | en_US |
| dc.subject | stress ulcer | en_US |
| dc.title | Effect of deferoxamine on ischemia/reperfusion in experimental stress ulceration | en_US |
| dc.type | article | en_US |
| dc.contributor.department | OMÜ | en_US |
| dc.identifier.volume | 23 | en_US |
| dc.identifier.issue | 4 | en_US |
| dc.identifier.startpage | 257 | en_US |
| dc.identifier.endpage | 261 | en_US |
| dc.relation.journal | Turkish Journal of Medical Sciences | en_US |
| dc.relation.publicationcategory | Makale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı | en_US |
