The pathophysiology of
cold injury is still controversial. An inflammatory process has been implicated as the underlying mechanism and certain anti-inflammatory substances such as
ibuprofen and
acetylsalicylic acid have been used in the clinical treatment of
frostbite injury. It has been postulated that the progressive ischemic
necrosis is secondary to excessive
thromboxane A2 production, which upsets the normal balance between
prostacyclin (
prostaglandin I2) and
thromboxane A2. It was aimed to clarify the pathophysiology of
cold injury in this study. Twenty-one New Zealand White rabbits, each weighing 1.2 to 2.9 kg, were divided into control (n = 10) and frostbitten (n = 11) groups the randomly. The rabbit ears in the frostbitten group were subjected to
cold injury, and the levels of
thromboxane A2 (as
thromboxane B2) and of
prostaglandin I2 (as 6-keto-prostaglandin F1alpha) and the number of inflammatory cells (polymorphonuclear leukocytes and mast cells) were measured in normal and frostbitten skin of rabbit ears. The levels of 6-keto
prostaglandin F1alpha and
thromboxane B2, the stable metabolites of
prostaglandin I2 and
thromboxane A2, respectively, were increased in a statistically significant way (p < 0.002) by
frostbite injury; however,
thromboxane B2 increased more than 6-keto
prostaglandin F1alpha. Polymorphonuclear leukocytes and mast cells, absent in normal skin, were present in the frostbitten skin. There was a statistically significant (p < 0.01) correlation between the time a rabbit ear was maintained at below -10 degrees C and skin survival and between the weights of rabbits and skin survival (p < 0.024). All these findings suggest that
inflammation is involved in
frostbite injury; a decrease in
prostaglandin I2/
thromboxane A2 ratio could be one of the factors leading to
necrosis; the bigger the animal, the better its ability to counter
frostbite.