DEFIBROTIDE ACTIVITY IN EXPERIMENTAL FROSTBITE INJURY

The pathogenesis of frostbite injury has not been completely elucidate d although the available evidence suggests it is an inflammatory react ion following reperfusion injury. Defibrotide given i.p, at 40 mg/kg/ day for three days to rabbits, the ears of which were subjected to fro stbite, decreased the presence of inflammatory cells (mast cells -76%; neutrophils -40.4%) and increased prostaglandin I-2 (PGI(2)) (as 6-Ke to-PGF(1 alpha)) in the involved skin. Thromboxane A(2) (TxA(2)) (as T xB(2)) was unaffected. These data strengthen the view that an inflamma tory process is the underlying cause of frostbite injury and that Defi brotide is active in pathological situations involving an inflammatory process like in frostbite.