Defibrotide activity in experimental frostbite injury

• Published in: British journal of plastic surgery 1998-09, Vol.51 (6), p.450-454
• Main Authors: Özyazgan, rfan, Günay, Galip K., Tercan, Mustafa, Bekerecilu, Mehmet, Melli, Mehmet, Üstün, Hüseyin
• Format: Article
• Language: English
• Subjects: 6-Ketoprostaglandin F1 alpha - metabolism; Animals; Biological and medical sciences; Female; Fibrinolytic Agents - therapeutic use; Frostbite - drug therapy; Frostbite - metabolism; Frostbite - pathology; Injuries of the skin. Diseases of the skin due to physical agents; Leukocyte Count; Male; Mast Cells - pathology; Medical sciences; Neutrophils - pathology; Platelet Aggregation Inhibitors - therapeutic use; Polydeoxyribonucleotides - therapeutic use; Rabbits; Skin - metabolism; Skin - pathology; Thromboxane A2 - metabolism; Traumas. Diseases due to physical agents
• ISSN: 0007-1226; 1465-3087
• DOI: 10.1054/bjps.1997.0061

The 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 I 2 (PGI 2) (as 6-Keto-PGF 1α) in the involved skin. Thromboxane A 2 (TxA 2) (as TxB 2) 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.