Eicosanoids and inflammatory cells in frostbitten tissue: prostacyclin, thromboxane, polymorphonuclear leukocytes, and mast cells.

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