Many experimental studies have been performed and the mechanism of hyperbaric oxygen therapy on the frostbitten tissue has not been elucidated. In this study, we evaluated the effect of hyperbaric oxygen therapy on the frostbitten ears of rabbits in an experimental animal model by examining the concentrations of thromboxane A2 (as thromboxane B2-Tx B2) and of prostaglandin I2 (PG I2) (as 6-keto-prostaglandin F1α-PG F1α) in tissues, and by counting the numbers of inflammatory cells (neutrophils and mast cells-MC) Hyperbaric oxygen therapy (HBO) at 2.5 ATA for 90 minutes twice daily for fourteen days to rabbits, the ears of which were subjected to frostbite, decreased presence of inflammatory cells (mast cells −75%; neutrophils −40%) and increased prostaglandin I2 (PG I2) (as 6-Keto-PGF1α) in the involved skin. Thromboxane A2 (TxA2) (as Tx B2) was unaffected. Our results revealed that an inflammatory process was the underlying cause of frostbite injury and that hyperbaric oxygen therapy was active in pathological situations involving an inflammatory process in frostbite.
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