Özyazgan I.Tercan M.Bekerecio?lu M.Melli M.Üstün H.Günay G.K.2024-08-042024-08-0419980007-1226https://doi.org/10.1054/bjps.1997.0061https://hdl.handle.net/11616/90361The pathogenesis of frostbite injury has not been completely elucidated although the available evidence suggests it is an inflammatory reaction following reperfusion injury. Defibrotide given i.p. at 40 mg/kg/day for three days to rabbits, the ears of which were subjected to frostbite, decreased the presence of inflammatory cells (mast cells -76%; neutrophils -40.4%) and increased prostaglandin I2 (PGI2) (as 6-Keto-PGF(1?)) in the involved skin. Thromboxane A2 (TxA2) (as TxB2)was unaffected. These data strengthen the view that an inflammatory process is the underlying cause of frostbite injury and that Defibrotide is active in pathological situations involving an inflammatory process like in frostbite.eninfo:eu-repo/semantics/closedAccess6 oxoprostaglandin F1 alphadefibrotideprostacyclinthromboxane A2thromboxane B2animal experimentanimal modelanimal tissuearticlecold injurycontrolled studyfemaleinflammationintraperitoneal drug administrationmalemast cellneutrophilnonhumanpathogenesispriority journalrabbitreperfusion injuryArticle516450454984936510.1054/bjps.1997.00612-s2.0-0032168583N/A