thromboxane-b2 and Frostbite

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.

Topics: 6-Ketoprostaglandin F1 alpha; Animals; Epoprostenol; Frostbite; Mast Cells; Neutrophils; Rabbits; Skin; Thromboxane A2; Thromboxane B2

The changes of some factors of blood coagulation system in rats following frost-bite of both hind feet under hypoxia were investigated. Male Wistar rats weighed 200 +/- 20g were divided into four groups: normal control (C); frostbite at normoxia (FN); frostbite during acute hypoxia (FAH) and frostbite during hypoxia after altitude acclimation (FHAC). Bleeding time and clotting time, rate of clot-retraction, plasma content of 6-keto-PGF1 alpha and TXB2 were determined following exposure to cold. The results showed that bleeding time and clotting time were shortened, and rate of clot-retraction was decreased, plasma content of 6-keto-PGF1 alpha and TXB2, T/P ratio were increased significantly after exposure to cold in all frostbite groups, but these changes were more prominent in FHAC than those in FN and FAH. The results demonstrated that there were changes in blood coagulation system following cold injury, blood coagulability was increased. These changes were closely related to the degree of frostbite. In addition, the degree of cold injury was aggravated by altitude acclimation and this may play an important role in the pathological process of dysfunction leading to necrosis of local frostbite tissue.

Topics: Acclimatization; Adaptation, Physiological; Animals; Blood Coagulation; Blood Coagulation Factors; Cold Temperature; Frostbite; Hypothermia, Induced; Hypoxia; Male; Oxygen; Prostaglandins F; Rats; Rats, Wistar; Thromboxane B2

Observations on early pathophysiology of burning suggests that the release of prostaglandins and thromboxanes plays a role in dermal ischemia. Because of the similarities of the early-phase frostbite wound, blister fluids were aspirated from 10 patients with frostbite, and routine biochemical analysis, immunoelectrophoresis, immunodiffusion, and evaluation of prostaglandins E2, F2 alpha, and thromboxane B2 were performed. Potassium, serum glutamic-oxaloacetic transaminase (SGOT), creatine phosphokinase (CPK), and lactic dehydrogenase (LDH) levels exceeded normal serum values. All blisters were found to have IgM, IgG, IgA, C3a, and opsonin. PgE2 was present in levels less than normal, but PgF2 alpha and TxB2 were markedly elevated. Since the vasoconstricting metabolites of arachidonic acid, PgF2 alpha and TxB2, are known to mediate dermal ischemia in burns and pedicle flaps, it is suggested they may play a role in the pathogenesis of frostbite.

Topics: Aspartate Aminotransferases; Aspartic Acid; Blister; Creatine; Creatine Kinase; Exudates and Transudates; Frostbite; Hand Injuries; Humans; Immunoglobulins; L-Lactate Dehydrogenase; Lactates; Potassium; Prostaglandins E; Thromboxane B2