Burn-Induced Alterations in Feeding, Energy Expenditure, and Brain Amine Neurotransmitters in Rats

Possible role of CRF peptides in burn-induced hypermetabolism

“…These rats were adapted to the laboratory environment for one week, and, except for pair-fed (PF) rats, were maintained on rat chow and tap water ad libitum. Following the adaptation period, the rats were anesthetized (ketamine/xylazine: 85 / 15 mg/kg, im; Phoenix Scientific, St. Joseph, MO; Butler Co., Dublin, OH) and subjected to 30% body surface area (BSA), full-thickness, open flame burn of 25 s duration, as we have described previously (Chance et al, 1987). Five minutes prior to the burn treatment, each rat was given fluid replacement therapy by injecting lactated Ringers solution (10 ml / 100 g BW, ip).…”

“…The PF control is necessary because rats typically exhibit a 3-day period of anorexia following major burn trauma. Resting energy expenditure was determined in all rats for 60 min as reported (Chance et al, 1987) by indirect calorimetry using an OXYMAX system (Columbus Instruments, Columbus, OH) at 1, 3 or 21 days postburn. Following these measurements, burned and FF rats were euthanized by decapitation, while the PF rats were euthanized the following day.…”

“…Thus, in both rats and guinea pigs, we reported (Chance et al, 1985(Chance et al, , 1987 reduced intake of chow for three to five days following a 30% body surface area (BSA), full-thickness burn. Therefore, elucidation of the neurochemical mediators of burn-induced hypermetabolism and anorexia may suggest new treatments and better nutritional management of burned patients.…”

Burn injury enhances brain prostaglandin E2 production through induction of cyclooxygenase-2 and microsomal prostaglandin E synthase in cerebral vascular endothelial cells in rats

“…P eripheral tissue burns often cause systemic reactions, such as fever (1,2), hyperalgesia (3,4), anorexia (5,6), and activation of the hypothalamo-pituitary-adrenal (HPA) axis (7,8), all of which are under the control of the central nervous system. An excess of these systemic reactions may lower the quality of life of patients and may enhance complications or mortality rate.…”

Mediation of burn-induced hypermetabolism by CRF receptor-2 activity

“…Although survival of major thermal injury depends upon several factors, including stabilization of the patient, management of shock, and preventing infection, the development of hypermetabolism causes nutritional management to be a significant problem for most of the recovery period (Wilmore et al, 1974). Burn-induced hypermetabolism is directly related to the extent of the burn injury (Wilmore et al, 1974), and nutritional status may be compromised further by a period of anorexia that typically follows major burn trauma (Chance et al, 1985(Chance et al, , 1987a. Therefore, better clinical management of burn patients may be achieved if the neurochemical mediators of hypermetabolism were known and controllable.…”