T HE PHYSIOLOGICAL and surgical literature of the past 30 years has reflected an intense interest in the metabolic reactions that follow the fracture of a major bone. It is now clear that in the presence of such severe injuries the body enters a phase of extensive tissue catabolism.3-5 The urinary excretion of large amounts of various products of protein breakdown leads to negative nitrogen balance in the well-nourished individual. Decreased glucose tolerance may develop and body fat is rapidly consumed in the early days after the trauma.5,8,10 This initial breakdown reaction is followed by a prolonged period in which protein containing tissues and fat deposits are restored to their prefracture state.7
While a considerable body of data has been accumulated to document widespread metabolic change in the postfracture period, there is very little information available concerning the nature and extent of the biochemical reactions of the
WRAY JB. Fracture in the Rat: Chronic Muscle Glycogen and Bone Change. Arch Surg. 1965;90(1):17–21. doi:10.1001/archsurg.1965.01320070019004
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