الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Surgery induces a variety of metabolic, hormonal, and inflammatory changes known as ”surgical stress response”, which may lead to prolonged in-hospital stay. The clinical manifestations of this reaction include post-operative complications such as respiratory failure, wound infections, myocardial damage with contractile dysfunction, renal impairment, coagulopathy, neurologic dysfunction and altered liver function with an increased mortality.
Inflammatory response in cardiac surgical patients is produced by complex interactions with numerous pathways including generation or activation of complements, cytokines, neutrophils, thrombin, mast cells, and others multiple inflammatory mediators. CPB responses have often been compared with the pathophysiologic changes occurring in SIRS.
Cytokines are immune mediators that direct the inflammatory response to sites of injury and infection and are essential for wound healing. An exaggerated production of pro-inflammatory cytokines from the primary site of injury, however, can manifest systemically as haemodynamic instability or metabolic derangements. IL-6 is a main pro-inflammatory cytokine produced as early as two to four hours after tissue damage. Circulating IL-6 levels appear to be proportional to the extent of tissue injury during an operation.
The metabolic effects of cortisol are directed to overcome the stressful state. Cortisol has widespread effects on the metabolism and utilization of glucose, amino acids and fatty acids in hepatic and extra-hepatic tissues.
Dexmedetomidine is an (α)-2 adrenergic agonist which is the pharmacologically active dextroisomer of medetomidine. It activates receptors in the medullary vasomotor center, reducing norepinephrine turnover and decreasing central sympathetic outflow, resulting in alterations in sympathetic function. Dexmedetomidine has significant analgesic qualities and has been labeled as ”analgesia-sparing” by the FDA. Because dexmedetomidine has no depressant effects on ventilation, its analgesic effect may offer a significant advantage for patients at risk for respiratory decompensation. One of the unique neuro-protective properties of dexmedetomidine is minimizing the incidence of delirium.