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.
Your session is about to expire. Do you want to continue logged in?
WARNING! You did not finish creating your certificate. Please click CONTINUE below to return to your previous page to complete the process. Failure to complete ALL the steps will result in a loss of this test score, and you will not receive credit for this course.