Eicosanoids and inflammatory cells in frostbitten tissue

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dc.authoridÖzyazgan, İrfan/0000-0003-2074-4587
dc.authorwosidOzyazgan, Irfan/U-6431-2018
dc.authorwosidÖzyazgan, İrfan/K-9601-2019
dc.contributor.authorÖzyazgan, I
dc.contributor.authorTercan, M
dc.contributor.authorMelli, M
dc.contributor.authorBekerecioglu, M
dc.contributor.authorÜstün, H
dc.contributor.authorGünay, GK
dc.date.accessioned2024-08-04T20:58:38Z
dc.date.available2024-08-04T20:58:38Z
dc.date.issued1998
dc.departmentİnönü Üniversitesien_US
dc.description.abstractThe pathophysiology of cold injury is still controversial. An inflammatory process has been implicated as the underlying mechanism and certain anti-inflammatory substances such as ibuprofen and acetylsalicylic acid have been used in the clinical treatment of frostbite injury. It has been postulated that the progressive ischemic necrosis is secondary to excessive thromboxane A(2) production, which upsets the normal balance between prostacyclin (prostaglandin Ig) and thromboxane A(2). It was aimed to clarify the pathophysiology of cold injury in this study. Twenty-one New Zealand White rabbits, each weighing 1.2 to 2.9 kg, were divided into control (n = 10) and frost bitten (n = 11) groups the randomly. The rabbit ears in the frostbitten group were subjected to cold injury, and the levels of thromboxane A(2) (as thromboxane B-2) and of prostaglandin I-2 (as 6-keto-prostaglandin F-1 alpha) and the number of inflammatory cells (polymorphonuclear leukocytes and mast cells) were measured in normal and frostbitten skin of rabbit ears. The levels of 6-keto prostaglandin F-1 alpha and thromboxane B-2, the stable metabolites of prostaglandin I-2 and thromboxane A(2), respectively, were increased in a statistically significant way (p < 0.002) by frostbite injury; however, thromboxane B-2 increased more than 6-keto prostaglandin F-1 alpha. Polymorphonuclear leukocytes and mast cells, absent in normal skin, were present in the frostbitten skin. There was a statistically significant (p < 0.01) correlation between the time a rabbit ear was maintained at below -10 degrees C and skin survival and between the weights of rabbits and skin survival (p < 0.024). All these findings suggest that inflammation is involved in frostbite injury; a decrease in prostaglandin I-2/thromboxane A(2) ratio could be one of the factors leading to necrosis; the bigger the animal, the better its ability to counter frostbite.en_US
dc.identifier.endpage1886en_US
dc.identifier.issn0032-1052
dc.identifier.issue7en_US
dc.identifier.pmid9623831en_US
dc.identifier.startpage1881en_US
dc.identifier.urihttps://hdl.handle.net/11616/103031
dc.identifier.volume101en_US
dc.identifier.wosWOS:000074010700016en_US
dc.identifier.wosqualityQ2en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherLippincott Williams & Wilkinsen_US
dc.relation.ispartofPlastic and Reconstructive Surgeryen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectCold Injuryen_US
dc.subjectSkinen_US
dc.subjectAnalogen_US
dc.subjectProstaglandinsen_US
dc.subjectInhibitionen_US
dc.subjectIschemiaen_US
dc.subjectRabbitsen_US
dc.subjectDrugsen_US
dc.subjectHanden_US
dc.titleEicosanoids and inflammatory cells in frostbitten tissueen_US
dc.typeArticleen_US

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