Interleukin-6 and Inflammatory Response in Cardiosurgery

Summary

The article presents basic information regarding the role of interleukin-6 in the pathogenesis of inflammatory response both at systemic and local levels with special emphasis on the myocardial reperfusion injury in cardiac surgical patients. A properly mounted inflammatory response is a condition sine qua non for the compromised host to survive. After the immediate danger has worn off, the inflammatory response proceeds to take over the control of healing and reparative processes. Proinflammatory cytokines start off the inflammation by inducing the up-regulation and de novo synthesis of adhesion molecules on the outer membrane of leukocytes and endothelial cells and by increasing the production of nitric oxide via the cytokine-inducible isoenzyme NO-synthase. When properly controlled, these changes of non-specific cell-mediated immunity prevent systemic dissemination of pathogenic microorganisms and help to destroy them as early as the latter have overcome the dermal or mucosal barriers. In addition, increased production of NO helps to maintain blood fluidity in conditions of activated coagulation and suppressed fibrinolysis which form an integral part of the defense reaction seeking to enclose the invading microbes within the inflammatory focus. Any shift of the equilibrium between the positive and negative feedback loops that control the inflammatory response leads to an insufficient or an exaggerated reaction. Typically, an inapropriate inflammatory response accounts for the low vascular resistance syndrome including its ready transition to an overt circulatory shock mediated by excessive production of nitric oxide. Among the proinflammatory cytokines, IL-6 plays the most important role in inducing systemic responses, i.e. the metabolic and neuroendocrine changes associated with the acute stress reaction. At the local level, IL-6 is an active participant in myocardial reperfusion injury. Later on IL-6 seems to be central in maintaining the function of the myocardium which has sustained damage during ischaemia-reperfusion, thus helping the host to survive.

Key words:
interleukin-6 - myocardium - inflammatory response - ischaemia - reperfusion