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      Effect of intraoperative infusion of dexmedetomidine on postoperative recovery in patients undergoing endovascular interventional therapies: A prospective, randomized, controlled trial

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          Abstract

          Background

          Rapid emergence from general anesthesia during endovascular interventional therapies (EITs) is important. However, the solution that improved quality of both analepsia and postoperative recovery after EITs has not been specifically addressed. We conducted this prospective, randomized, controlled trial to evaluate the intraoperative infusion of dexmedetomidine on quality of analepsia and postoperative recovery in patients undergoing EITs.

          Methods

          Eighty‐six patients undergoing EITs were divided into three groups: RD1 (dexmedetomidine at an initial dose of 0.5 μg/kg for 10 min adjusted to 0.2 μg kg −1 hr −1 throughout EIT), RD2 (dexmedetomidine at an initial dose of 0.5 μg/kg for 10 min adjusted to 0.4 μg kg −1 hr −1 throughout EIT), and RD3 (dexmedetomidine at an initial dose of 0.5 μg/kg for 10 min adjusted to 0.6 μg kg −1 hr −1 throughout EIT). An analgesia system delivered sufentanil only. The primary outcome measure was the total consumption of nimodipine during the first 48 hr after surgery. The secondary outcome measures were sufentanil consumption, pain intensity, hemodynamics, functional activity score (FAS), neurologic examination, level of sedation (LOS), and Bruggrmann comfort scale (BCS). We also recorded the intraoperative hemodynamic data, requirement of narcotic and vasoactive drugs, prevalence of complications and symptomatic cerebral vasospasm, duration of postanesthesia care unit (PACU) stay, Glasgow Outcome Score (GOS) at 3 months, and prevalence of cerebral infarction 30 days after surgery.

          Results

          Dexmedetomidine application in the regimen RD3 reduced the consumption of the total dose of nimodipine and sufentanil 48 hr after surgery, prevalence of symptomatic cerebral vasospasm, consumption of narcotic drugs and nimodipine during surgery, pain intensity during the first 8 hr after surgery, and increased both BCS during the first 4 hr after surgery and hemodynamic stability. However, the LOS was increased at the 0.5 hr after surgery and surgeon satisfaction score was lower. There were no significant differences among the groups for consumption of vasoactive drugs except urapidil, Glasgow coma scale (GCS) and FAS during the first 48 hr after surgery, GOS at 3 months, and cerebral infarction after 30 days.

          Conclusions

          Dexmedetomidine (an initial dose of 0.5 μg/kg for 10 min adjusted to 0.6 μg kg −1 hr −1 throughout EIT) could reduce the total consumption of nimodipine and opioid during the first 48 hr after surgery, the concerning adverse effects, and improve pain scores. The optimal dosage of dexmedetomidine during EITs merits further investigation.

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          Most cited references43

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          Dexmedetomidine: a review of clinical applications.

          The present review serves as an overview update in the diverse uses of the sedative dexmedetomidine. Dexmedetomidine is a selective alpha2 adrenoreceptor agonist that has been described as a useful, safe adjunct in many clinical applications. This paper reviews current clinical uses, mechanism of action, and side effects of dexmedetomidine. The current uses reviewed include sedation in the ICU (adult and pediatric), neurosurgery, pediatric procedural sedation, awake fiber-optic intubation, cardiac surgery, and bariatric surgery. Dexmedetomidine is a useful medication with many clinical applications. The medication has shown efficacy in decreasing the need for opioids, benzodiazepines, propofol, and other sedative medications. Short-term sedation has been shown to be safe in studies, although hypotension and bradycardia are the most significant side effects. Dexmedetomidine has been used effectively for sedation during pediatric procedures and in the ICU. In order to reduce sympathetic tone during cardiac surgery, a low-dose dexmedetomidine infusion has been utilized. The bariatric surgery population has also been studied with dexmedetomidine because of its adequate sedation and less prevalent respiratory depression when compared with opioid administration. Dexmedetomidine is emerging as an effective therapeutic agent in the management of a wide range of clinical conditions with an efficacious, safe profile.
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            Paroxysmal sympathetic hyperactivity after acquired brain injury: consensus on conceptual definition, nomenclature, and diagnostic criteria.

            A syndrome of paroxysmal, episodic sympathetic hyperactivity after acquired brain injury has been recognized for almost 60 years. This project sought to simplify the confused nomenclature for the condition (>31 eponyms) and simplify the nine overlapping sets of diagnostic criteria. A consensus-developed questionnaire based on a systematic review of the literature was circulated to a widely representative, international expert group utilizing a Delphi approach. Diagnostic criteria were dropped if group consensus failed to agree on their relative importance, with a goal of reaching a Cronbach α of 0.8 (suitable for research purposes). The resulting criteria were combined into an assessment measure for clinical and research settings. The consensus group recommend that the term "paroxysmal sympathetic hyperactivity" replace previous terms to describe the "syndrome, recognised in a subgroup of survivors of severe acquired brain injury, of simultaneous, paroxysmal transient increases in sympathetic [elevated heart rate, blood pressure, respiratory rate, temperature, sweating] and motor [posturing] activity." An 11 point probabilistic diagnostic scale was developed with reference to published criteria, yielding an acceptable Cronbach α of 0.8. These 11 items were proceduralized and combined with a symptom severity index to produce a diagnostic tool for use with adults (the paroxysmal sympathetic hyperactivity assessment measure [PSH-AM]). Development of a pediatric version of the scale and further research into the validity of the PSH-AM is recommended. The consensus position builds on previous literature to establish diagnostic definitions and criteria, an important move to standardize research and management of this condition.
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              Dexmedetomidine Protects Mouse Brain from Ischemia-Reperfusion Injury via Inhibiting Neuronal Autophagy through Up-Regulating HIF-1α

              Stroke is the leading cause of death in China and produces a heavy socio-economic burden in the past decades. Previous studies have shown that dexmedetomidine (DEX) is neuroprotective after cerebral ischemia. However, the role of autophagy during DEX-mediated neuroprotection after cerebral ischemia is still unknown. In this study, we found that post-conditioning with DEX and DEX+3-methyladenine (3-MA) (autophagy inhibitor) reduced brain infarct size and improved neurological deficits compared with DEX+RAPA (autophagy inducer) 24 h after transient middle cerebral artery artery occlusion (tMCAO) model in mice. DEX inhibited the neuronal autophagy in the peri-ischemic brain, and increased viability and decreased apoptosis of primary cultured neurons in oxygen-glucose deprivation (OGD) model. DEX induced expression of Bcl-1 and p62, while reduced the expression of microtubule-associated protein 1 light chain 3 (LC3) and Beclin 1 in primary cultured neurons through inhibition of apoptosis and autophagy. Meanwhile, DEX promoted the expression of hypoxia-inducible factor-1α (HIF-1α) both in vivo and in vitro, and 2-Methoxyestradiol (2ME2), an inhibitor of HIF-1α, could reverse DEX-induced autophagic inhibition. In conclusion, our study suggests that post-conditioning with DEX at the beginning of reperfusion protects mouse brain from ischemia-reperfusion injury via inhibition of neuronal autophagy by upregulation of HIF-1α, which provides a potential therapeutic treatment for acute ischemic injury.
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                Author and article information

                Contributors
                zwzhang68@sina.com
                caojl0310@aliyun.com
                Journal
                Brain Behav
                Brain Behav
                10.1002/(ISSN)2157-9032
                BRB3
                Brain and Behavior
                John Wiley and Sons Inc. (Hoboken )
                2162-3279
                17 May 2019
                July 2019
                : 9
                : 7 ( doiID: 10.1002/brb3.2019.9.issue-7 )
                : e01317
                Affiliations
                [ 1 ] Jiangsu Province Key Laboratory of Anesthesiology Xuzhou Medical University Xuzhou China
                [ 2 ] Jiangsu Province Key Laboratory of Anesthesia and Analgesia Application Technology Xuzhou Medical University Xuzhou China
                [ 3 ] Department of Anesthesiology Liaocheng People's Hospital Liaocheng Shandong China
                [ 4 ] Department of Anesthesiology The Affiliated Hospital of Xuzhou Medical University Xuzhou China
                Author notes
                [*] [* ] Correspondence

                Jun-Li Cao, Jiangsu Province Key Laboratory of Anesthesiology, Xuzhou Medical University, Xuzhou, China.

                Email: caojl0310@ 123456aliyun.com

                Zongwang Zhang, Department of Anesthesiology, Liaocheng People's Hospital, Liaocheng, Shandong, China.

                Email: zwzhang68@ 123456sina.com

                Author information
                https://orcid.org/0000-0002-3404-8382
                Article
                BRB31317
                10.1002/brb3.1317
                6625481
                31099992
                82690ec9-6e93-4d3a-8b20-8c68f0057f45
                © 2019 The Authors Brain and Behavior Published by Wiley Periodicals, Inc.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                : 12 March 2019
                : 25 April 2019
                : 27 April 2019
                Page count
                Figures: 8, Tables: 6, Pages: 12, Words: 7814
                Funding
                Funded by: Natural Science Foundation of Shandong Province
                Award ID: ZR2016HB28
                Categories
                Original Research
                Original Research
                Custom metadata
                2.0
                brb31317
                July 2019
                Converter:WILEY_ML3GV2_TO_NLMPMC version:5.6.5 mode:remove_FC converted:12.07.2019

                Neurosciences
                cerebral vasospasm,dexmedetomidine,endovascular interventional therapies,neuroanesthesia,nimodipine

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