Defibrotide activity in experimental frostbite injury
Küçük Resim Yok
Tarih
1998
Dergi Başlığı
Dergi ISSN
Cilt Başlığı
Yayıncı
Churchill Livingstone
Erişim Hakkı
info:eu-repo/semantics/closedAccess
Özet
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-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.
Açıklama
Anahtar Kelimeler
6 oxoprostaglandin F1 alpha, defibrotide, prostacyclin, thromboxane A2, thromboxane B2, animal experiment, animal model, animal tissue, article, cold injury, controlled study, female, inflammation, intraperitoneal drug administration, male, mast cell, neutrophil, nonhuman, pathogenesis, priority journal, rabbit, reperfusion injury
Kaynak
British Journal of Plastic Surgery
WoS Q Değeri
Scopus Q Değeri
N/A
Cilt
51
Sayı
6
