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      Protective effect of dexmedetomidine in coronary artery bypass grafting surgery

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          Abstract

          The aim of this study was to observe the impact of dexmedetomidine on postoperative myocardial injury in patients undergoing off-pump coronary artery bypass (OPCAB) grafting. One hundred and sixty-two patients who were undergoing OPCAB surgery were randomly divided into control and dexmedetomidine groups (groups C and Dex, respectively). Following the first vascular anastomosis grafting, the patients in group Dex received a continuous intravenous infusion of 0.2–0.5 μg/kg/h dexmedetomidine, until they were transferred to the Cardiac Surgery intensive care unit (ICU) for 12 h. Patients in group C received physiological saline intraoperatively and an intravenous infusion of 2–4 mg/kg/h isopropylphenol for postoperative sedation. Invasive arterial pressure and heart rate were continuously monitored for 5 min subsequent to entry into the operating theatre (T0), immediately following surgery (T1), 12 h post-surgery (T2), 24 h post-surgery(T3), 48 h post-surgery(T4) and 72 h post-surgery (T5). Blood samples were taken to determine the plasma levels of cardiac troponin I (cTnI) and creatine kinase-MB (CK-MB) at each time point. At 72 h post-surgery, a dynamic electrocardiogram was monitored. The blood pressure, heart rate, levels of cTnI, CK-MB, norepinephrine and cortisol, and postoperative arrhythmic events in the patients in group Dex all decreased compared with those in group C. The duration of mechanical ventilation and ICU residence time were also shorter than those in the control group (P<0.05). Dexmedetomidine reduced post-surgical myocardial injury in patients who had undergone OPCAB surgery.

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          The effects of increasing plasma concentrations of dexmedetomidine in humans.

          This study determined the responses to increasing plasma concentrations of dexmedetomidine in humans. Ten healthy men (20-27 yr) provided informed consent and were monitored (underwent electrocardiography, measured arterial, central venous [CVP] and pulmonary artery [PAP] pressures, cardiac output, oxygen saturation, end-tidal carbon dioxide [ETCO2], respiration, blood gas, and catecholamines). Hemodynamic measurements, blood sampling, and psychometric, cold pressor, and baroreflex tests were performed at rest and during sequential 40-min intravenous target infusions of dexmedetomidine (0.5, 0.8, 1.2, 2.0, 3.2, 5.0, and 8.0 ng/ml; baroreflex testing only at 0.5 and 0.8 ng/ml). The initial dose of dexmedetomidine decreased catecholamines 45-76% and eliminated the norepinephrine increase that was seen during the cold pressor test. Catecholamine suppression persisted in subsequent infusions. The first two doses of dexmedetomidine increased sedation 38 and 65%, and lowered mean arterial pressure by 13%, but did not change central venous pressure or pulmonary artery pressure. Subsequent higher doses increased sedation, all pressures, and calculated vascular resistance, and resulted in significant decreases in heart rate, cardiac output, and stroke volume. Recall and recognition decreased at a dose of more than 0.7 ng/ml. The pain rating and mean arterial pressure increase to cold pressor test progressively diminished as the dexmedetomidine dose increased. The baroreflex heart rate slowing as a result of phenylephrine challenge was potentiated at both doses of dexmedetomidine. Respiratory variables were minimally changed during infusions, whereas acid-base was unchanged. Increasing concentrations of dexmedetomidine in humans resulted in progressive increases in sedation and analgesia, decreases in heart rate, cardiac output, and memory. A biphasic (low, then high) dose-response relation for mean arterial pressure, pulmonary arterial pressure, and vascular resistances, and an attenuation of the cold pressor response also were observed.
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            Dexmedetomidine: an updated review.

            To review recent literature on the safety and efficacy of dexmedetomidine. Articles were identified through searches of MEDLINE (1966-January 2007). Key words included dexmedetomidine, medetomidine, alpha(2)-agonist, and sedation. References from selected articles were reviewed for additional references. Experimental and observational studies that focused on the safety and efficacy of dexmedetomidine in humans were selected. Dexmedetomidine is an alpha(2)-agonist for short-term sedation in critically ill patients. In postoperative patients, dexmedetomidine produced similar levels of sedation and times to extubation, with less opioid requirements compared with propofol. Dexmedetomidine has also been studied for sedation in critically ill medical and pediatric patients, as adjunct to anesthesia, and for procedural sedation. Hypotension, hypertension, and bradycardia are common adverse effects. Although dexmedetomidine is labeled only for sedation less than 24 hours, it has been administered for longer than 24 hours without apparent development of rebound hypertension and tachycardia. Dexmedetomidine is a safe and effective agent for sedation in critically ill patients. Further, well designed studies are needed to define its role as a sedative for critically ill medical, neurosurgical, and pediatric patients, as an adjunct to anesthesia, and as a sedative during procedures.
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              Effect of dexmedetomidine on haemodynamic responses to laryngoscopy and intubation : perioperative haemodynamics and anaesthetic requirements.

              Dexmedetomidine reduces the dose requirements for opioids and anaesthetic agents. The purpose of this study was to evaluate the effect of a single pre-induction intravenous dose of dexmedetomidine 1 microg/kg on cardiovascular response resulting from laryngoscopy and endotracheal intubation, need for anaesthetic agent and perioperative haemodynamic stability. Fifty patients scheduled for elective minor surgery were randomised into two groups (dexmedetomidine group and placebo group, n = 25 in each group). During and after drug administration, the Ramsey sedation scale was applied every 5 minutes. Fentanyl 1 microg/kg was administered to all patients and thiopental was given until lash reflex disappeared. Anaesthesia continuation was maintained with 50% : 50%, oxygen : nitrous oxide. Sevoflurane concentration was adjusted to maintain systolic blood pressure within 20% of preoperative values. After extubation, the Steward awakening score was applied at 5 and 10 minutes. Haemodynamic parameters and adverse effects were recorded every 10 minutes for 1 hour after surgery. During intubation the need for thiopental and sevoflurane concentration were decreased by 39% and 92%, respectively, in the dexmedetomidine group compared with the placebo group. In all groups, blood pressure and heart rate increased after tracheal intubation; both were significantly lower in the dexmedetomidine group than in the placebo group (p 6 in 56% of the dexmedetomidine group and in 4% of the placebo group (p or =4 in all patients in the dexmedetomidine group (p < 0.05). Arterial blood pressure and heart rate in the postoperative period were significantly lower in the dexmedetomidine group compared with the placebo group (p < 0.05). Preoperative administration of a single dose of dexmedetomidine resulted in progressive increases in sedation, blunted the haemodynamic responses during laryngoscopy, and reduced opioid and anaesthetic requirements. Furthermore, dexmedetomidine decreased blood pressure and heart rate as well as the recovery time after the operation.
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                Author and article information

                Journal
                Exp Ther Med
                Exp Ther Med
                ETM
                Experimental and Therapeutic Medicine
                D.A. Spandidos
                1792-0981
                1792-1015
                August 2013
                25 June 2013
                25 June 2013
                : 6
                : 2
                : 497-502
                Affiliations
                [1 ]Department of Anesthesiology, The Second Affiliated Hospital, Hebei Medical University, Shijiazhuang, Hebei 050000;
                [2 ]Dezhou Institute for Drug Control, Dezhou, Shandong 253015, P.R. China
                Author notes
                Correspondence to: Dr Zhenming Dong, Department of Anesthesiology, The Second Affiliated Hospital, Hebei Medical University, No.215 Hepingxi Road, Shijiazhuang, Hebei 050000, P.R. China, E-mail: jjdoccn@ 123456yeah.net
                Article
                etm-06-02-0497
                10.3892/etm.2013.1183
                3786847
                24137215
                b7de0e3f-2468-48a8-9d44-9bc3fd16c161
                Copyright © 2013, Spandidos Publications

                This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.

                History
                : 09 March 2013
                : 03 June 2013
                Categories
                Articles

                Medicine
                dexmedetomidine,hemodynamics,cardiac function,myocardial reperfusion injury,coronary artery bypass grafting,off-pump

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