Abstract

Despite the fact that coronary artery bypass grafting surgery (CABG) with cardiopulmonary bypass (CPB) prolongs life and reduces symptoms in patients with severe coronary artery diseases, these benefits are accompanied by increased risks. Morbidity associated with cardiopulmonary bypass can be attributed to the generalized inflammatory response induced by blood-xenosurfaces interactions during extracorporeal circulation and the ischemia/reperfusion implications, including exacerbated inflammatory response resembling the systemic inflammatory response syndrome (SIRS). The use of specific anesthetic agents with anti-inflammatory activity can modulate the deleterious inflammatory response. Consequently, anti-inflammatory anesthetics may accelerate postoperative recovery and better outcomes than classical anesthetics. It is known that the stress response to surgery can be attenuated by sympatholytic effects caused by activation of central (α-)2-adrenergic receptor, leading to reductions in blood pressure and heart rate, and more recently, that they can have anti-inflammatory properties. This paper discusses the clinical significance of the dexmedetomidine use, a selective (α-)2-adrenergic agonist, as a coadjuvant in general anesthesia. Actually, dexmedetomidine use is not in anesthetic routine, but this drug can be considered a particularly promising agent in perioperative multiple organ protection.

Highlights

  • Independent of leukocytes, production of toxic reactive oxygen species occurs, leading to release of arachidonic acid metabolites, proinflammatory cytokines by ischemic cells (e.g., plasma tumor necrosis factor-alpha and interleukins like IL-1, IL-6, and IL-8), and activation of the humoral protein systems [30]

  • Surgery induces a variety of metabolic, endocrine, and immune changes known as the “stress response,” which may lead to prolonged in-hospital stay

  • It was demonstrated that release of cytokines, such as tumor necrosis factor-alpha and interleukins, as mediated by oxidative stress and prolonged microglial activation by interleukin-1 induce to a neuronal degeneration that follow cerebral ischemia [49] and that excessive formation of reactive oxygen species induce to direct tissue damage and stimulate inflammatory and proapoptotic cascades [50]

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Summary

Introduction

Independent of leukocytes, production of toxic reactive oxygen species occurs, leading to release of arachidonic acid metabolites, proinflammatory cytokines by ischemic cells (e.g., plasma tumor necrosis factor-alpha and interleukins like IL-1, IL-6, and IL-8), and activation of the humoral protein systems [30]. The study indicates that, for the majority of low risk patients undergoing coronary artery bypass surgery, oxidative stress remains a constant underlying factor, unlikely to significantly influence clinical outcome as long as myocardial protection is provided and the ischemic duration is kept as short as possible.

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