Abstract

Acute pain is a prevalent and debilitating complication following burn injury and has the potential in certain individuals to become chronic pain. There is a paucity of preclinical and clinical research that has addressed this large clinical problem. Our recent work has been focused on developing a burn injury model that will allow for mechanistic investigations for acute and chronic burn injury pain. Our group has previously reported that mice given a high fat/rich carbohydrate diet (54% kcal from fat, 25% kcal from carbohydrate (CHO))develop mechanical allodynia. The present work sought to examine whether this high fat, high CHO diet may affect pain behaviors related to acute burn injury and whether it would lead to prolonged pain behaviors consistent with chronic burn pain. Mice were given either a normal chow or a high fat/high CHO diet and then either were given burn or sham injury on the right hind paw. Pain behaviors were observed over a 28 day period after the burn injury and included mechanical and thermal assessments. Results indicate that both normal chow and high fat diet burn injured mice exhibited significantly reduced mechanical pain thresholds for two weeks after burn injury. After 14 days, both burn injury groups displayed increased mechanical pain thresholds that by 28 days, were surprisingly higher than baseline. Overall, the high fat diet burn group was not found to display greater levels of allodynia compared to the normal chow burn group and there was no evidence that the current model or the high fat diet led to pain behaviors consistent with chronic pain. Preliminary investigations into proportions of mast cell degranulation show that burn injury led to a higher percentage of degranulated mast cells compared to sham injury and that dietary influence may also have a small impact.

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