E0000960

open access

Version of Record

The Relationship of IL-6 to Hormonal Mediators,Fuel Utilization,and Systemic Hypermetabolism after Surgical Trauma

English (英語)

The Kobe journal of the medical sciences

42(3)

187-205

1996-06

OBJECTIVES: To define the relationship between inflammatory cytokines, hormonal mediators, alteration of energy substrate and hypermetabolism during the early phase after surgical trauma. DESIGN: A prospective case-control study of 13 patients underwent elective surgery for carcinoma between November 1993 and January 1995. MATERIALS AND METHODS: They received parenteral supply of adequate glucose and amino acids through central venous catheter after surgery equally. Inflammatory cytokines such as TNF- alpha, IL-1 and IL-6, stress hormones such as norepinephrine, glucagon and insulin, and fuel utilization and hypermetabolism variables such as resting energy expenditure (REE), CRP, free fatty acid, respiratory quotient, the calculated rates of glucose and fat oxidation using indirect calorimetry were measured serially (the day before operation, the end of surgery, and postoperative day (POD) 1, 2 and 5). MEASUREMENTS AND MAIN RESULTS: TNF- alpha and IL-1 were not detected during the study period. Initial elevation and steady decline of IL-6 concentrations were seen after surgical injury, and this response related significantly to post-operative norepinephrine and glucagon levels throughout the study period, and to insulin levels only at the end of surgery. %REE (REE/BEEHB; basal energy expenditure according to the Harris-Benedict equation) on POD 2 and 5, and all CRP levels after surgery were significantly related to IL-6 levels more than hormone levels. Fuel utilization variables on POD 2 were related to both IL-6 and hormone levels. CONCLUSIONS: Initial elevation of IL-6 concentration might induce stress hormones such as norepinephrine and glucagon, but not insulin after surgical trauma. Moreover not only hormonal mediators but also cytokine such as IL-6 are responsible for the development of the stress response of the alteration of energy substrate and hypermetabolism.

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