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James M. Watters, MD, FRCS(C); Palmer Q. Bessey, MD; Charles A. Dinarello, MD; Sheldon M. Wolff, MD; Douglas W. Wilmore, MD

Arch Surg. 1986;121(2):179-190.

Abstract
• 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, hyperinsulinemia, 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.

(Arch Surg 1986;121:179-190)

Author Affiliations
From the Department of Surgery, Harvard Medical School and Brigham and Women's Hospital, Boston (Drs Watters, Bessey, and Wilmore); and the Department of Medicine, Tufts University School of Medicine, Boston (Drs Dinarello and Wolff).

Footnotes
Accepted for publication Oct 4, 1985.

Read before the Fifth Annual Meeting of the Surgical Infection Society, New Orleans, April 30, 1985.

Reprint requests to Department of Surgery, Brigham and Women's Hospital, 75 Francis St, Boston, MA 02115 (Dr Wilmore).

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