Modulating the metabolic response to injury and infection.

The host metabolic response to injury, be it defined as traumatic or infectious in nature, is characterized by diverse alterations in substrate turnover at the systemic and tissue levels (Lowry, 1986; Goldstein & Elwyn, 1989). Numerous studies attest to the extent of altered metabolic processes in injured and septic patient populations. For example, the isotopically determined rates of turnover for glucose, free fatty acids and of leucine emanating from the collaborative studies of Shaw and Wolfe (Shaw et al. 1985; Shaw & Wolfe, 1987; Wolfe et al. 1987; Jahoor et al. 1989) are presented in Table 1. Although a consensus of similar studies by other investigators notes a generalized increase in substrate turnover during the flow phase, such metabolic changes are dynamic in nature. Therefore, attention to the timing of such determinations in relation to the injury event as well as the severity and antecedent clinical management of the process is required.