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.