Defibrotide activity in experimental frostbite injury

Br J Plast Surg. 1998 Sep;51(6):450-4. doi: 10.1054/bjps.1997.0061.

Abstract

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 I2 (PGI2) (as 6-Keto-PGF1 alpha) 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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 6-Ketoprostaglandin F1 alpha / metabolism
  • Animals
  • Female
  • Fibrinolytic Agents / therapeutic use*
  • Frostbite / drug therapy*
  • Frostbite / metabolism
  • Frostbite / pathology
  • Leukocyte Count
  • Male
  • Mast Cells / pathology
  • Neutrophils / pathology
  • Platelet Aggregation Inhibitors / therapeutic use*
  • Polydeoxyribonucleotides / therapeutic use*
  • Rabbits
  • Skin / metabolism
  • Skin / pathology
  • Thromboxane A2 / metabolism

Substances

  • Fibrinolytic Agents
  • Platelet Aggregation Inhibitors
  • Polydeoxyribonucleotides
  • defibrotide
  • Thromboxane A2
  • 6-Ketoprostaglandin F1 alpha