EFFECT OF ENVIRONMENTAL TEMPERATURE ON THE METABOLIC RESPONSE TO INJURY

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Abstract
Male hooded rats of the Rowett Research Institute strain, maintained before and after experimental fracture of a femur at an environmental temperature of 30° C, with feed intake fixed at the pre‐injury level, generally failed to show the marked and characteristic increased urinary nitrogen excretion normally observed to follow such injury at room temperature (20°–22° C). There was also no rise in heat production following fracture at this higher temperature as measured in a gradient‐layer calorimeter, such as was previously noted to follow this form of injury at normal room temperature. The animals at the higher temperature on ad libitum feeding ate some 24 per cent less food following fracture and some 30 per cent less following incision. On ad libitum feeding the characteristic response to fracture or incision in the rat was generally much less marked, even apparently absent at 30° C and at 20° C. There was accompanying weight gain, but interpretation is complicated by a fall in intake following the injury. Whether reduction in food intake at the higher temperature is the main reason for the disappearance of the catabolic effect, or whether its removal is to reduce heat load, is not certain. Its apparent elimination at 20° C on ad libitum feeding may have the same origin. Fracture of the femur does not expose a wet surface such as is seen in burns and, in any case, even at normal room temperatures there was no increment in heat loss by evaporation following fracture to warrant an increase in heat production. It may be that a more probable explanation is that, if the increased demands for extra energy are met by increased food supply or rendered unnecessary by raising the environmental temperature, then body reserves are not called on for this purpose in order to reduce the heat load.