Systemic inflammatory response syndrome: a new direction?
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The inflammatory response to cardiac surgery is partially responsible of many postoperative complications like the systemic inflammatory response syndrome and the respiratory distress syndrome. The pathophysiology of the inflammatory response was widely studied and many inflammatory mediators have been detected. However, most of the studies focused on the systemic component of the inflammatory response without adequately considering the local cardiopericardiac reaction. The pericardium and edpicardiac adipose tissue can actively synthesize and secrete various mediators. It is highly possible that there is a correlation but the local and systemic types of inflammatory response. The aim of this study isto study and quantify the local cardiopericardiac component of the inflammatory response that follows cardiac surgery.
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Despite advances in the techniques of ‘off-pump’ Cardiac surgery, the vast majority of cardiac operations still involve using cardiopulmonary bypass (CPB) along with some form of myocardial protection. The extracorporeal circuits used in the modern bypass-machine have developed considerably in the last few decades. However contact activation of blood leading to a systemic inflammatory response is to some degree inevitable. Although often remaining sub-clinical and resolving promptly at the end of CPB, in its most extreme form this inflammatory response may be associated with the development of the systemic inflammatory response syndrome (SIRS) that can often lead to major organ dysfunction syndrome (MODs) and death. Here we review the pathophysiology behind the development of this “whole body” inflammatory response and consider the mechanical and pharmacological methods that are currently used to minimise it. Keywords: Inflammation, cardiopulmonary bypass, SIRS
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Systemic inflammatory response syndrome (SIRS) is a non-specific exaggerated defense response caused by infectious or non-infectious stressors such as trauma, burn, surgery, ischemia and reperfusion, and malignancy, which can eventually lead to an uncontrolled inflammatory response. In addition to the early mortality due to the “first hits” after trauma, the trauma-induced SIRS and multiple organ dysfunction syndrome (MODS) are the main reasons for the poor prognosis of trauma patients as “second hits”. Unlike infection-induced SIRS caused by pathogen-associated molecular patterns (PAMPs), trauma-induced SIRS is mainly mediated by damage-associated molecular patterns (DAMPs) including mitochondrial DAMPs (mtDAMPs). MtDAMPs released after trauma-induced mitochondrial injury, including mitochondrial DNA (mtDNA) and mitochondrial formyl peptides (mtFPs), can activate inflammatory response through multiple inflammatory signaling pathways. This review summarizes the role and mechanism of mtDAMPs in the occurrence and development of trauma-induced SIRS.
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