In response to tissue injury and cell death, cytokines (interleukins (IL-1, IL-6], tumor necrosis factors [TNF-α]) and other mediators of inflammation (eicosanoids, serotonin, histamine, and kinins) initiate the inflammatory response.1-3 The paracrine (i.e., local) response is characterized by the release of IL-1 and TNF-α from activated macrophages and monocytes followed by the production of IL-6. IL-6 is primarily responsible for endocrine and autocrine responses.
High concentrations of IL-6 associated with major surgical stress stimulate the secretion of cortisol and other stress hormones, and increase the release of epinephrine. Cortisol has well recognized anti-inflammatory effects mediated by a decrease in the production of inflammatory mediators. Consequently, cortisol acts to dampen the intensity of the inflammatory response to further calibrate the balance between pro-inflammatory and anti-inflammatory processes.
IL-6 concentrations, which peak 12 to 24 hours after surgery, reflect the degree of tissue damage associate with a procedure and along with other cytokines cause the production of acute phase proteins such as C-reactive protein (CRP). CRP participates in the clearance of necrotic and apoptotic cells. Measuring the CRP level is a useful screen for postoperative inflammation and is the main predictive factor of the patient’s physical condition after major surgery.