Both inflammatory and endocrine mediators stimulate host responses to sepsis
J. M. Watters, P. Q. Bessey, C. A. Dinarello, S. M. Wolff and D. W. Wilmore
Host responses to sepsis and trauma are complex and their mediators are not
well understood. To examine the roles of "endocrine" and "inflammatory"
mediators, we studied healthy volunteers in four experimental groups:
continuous 72-hour infusion of normal saline; continuous 72-hour infusion
of hydrocortisone, glucagon, and epinephrine; daily intramuscular injection
of the inflammatory agent etiocholanolone; and combined etiocholanolone
injection--hormone infusion. In this model hypermetabolism, hyperglycemia,
hyper-insulinemia, insulin resistance, negative nitrogen balance, and
accelerated protein flux were mediated predominantly by infusion of the
counterregulatory hormones. Etiocholanolone injection resulted in fever,
acute-phase--protein synthesis, and hypoferremia. Leukocyte, temperature,
and C-reactive--protein responses reflected major interactions between
these stimuli. Both inflammatory and endocrine mediators are necessary for
the complete manifestation of host responses to critical illness.
