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J A Tan - One of the best experts on this subject based on the ideXlab platform.
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use of dexmedetomidine as a Sedative and analgesic Agent in critically ill adult patients a meta analysis
Intensive Care Medicine, 2010Co-Authors: J A TanAbstract:To assess the effects of using dexmedetomidine as a Sedative and analgesic Agent on length of intensive care unit (ICU) stay, duration of mechanical ventilation, risk of bradycardia, and hypotension in critically ill adult patients. Two researchers searched MEDLINE, EMBASE, and the Cochrane controlled trial register independently for randomized controlled trials comparing dexmedetomidine with a placebo or an alternative Sedative Agent, without any language restrictions. A total of 2,419 critically ill patients from 24 trials were subject to meta-analysis. Dexmedetomidine was associated with a significant reduction in length of ICU stay [weighted mean difference −0.48 days, 95% confidence interval (CI) −0.18 to −0.78 days, P = 0.002], but not duration of mechanical ventilation, when compared with an alternative Sedative Agent. There was, however, significant heterogeneity in these two outcomes between the pooled studies. Dexmedetomidine was associated with increased risk of bradycardia requiring interventions in studies that used both a loading dose and maintenance doses >0.7 μg kg−1 h−1 [relative risk (RR) 7.30, 95% CI 1.73–30.81, P = 0.007]. Risks of hypotension requiring interventions (RR 1.43, 95% CI 0.78–2.6, P = 0.25), delirium (RR 0.79, 95% CI 0.56–1.11, P = 0.18), self-extubation, myocardial infarction, hyperglycemia, atrial fibrillation, and mortality were not significantly different between dexmedetomidine and traditional Sedative and analgesic Agents. Significant heterogeneity existed between the pooled studies. The limited evidence suggested that dexmedetomidine might reduce length of ICU stay in some critically ill patients, but the risk of bradycardia was significantly higher when both a loading dose and high maintenance doses (>0.7 μg kg−1 h−1) were used.
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use of remifentanil as a Sedative Agent in critically ill adult patients a meta analysis
Anaesthesia, 2009Co-Authors: J A TanAbstract:This meta-analysis examined the benefits of using remifentanil as a Sedative Agent in critically ill patients. A total of 11 randomised controlled trials, comparing remifentanil with another opioid or hypnotic Agent in 1067 critically ill adult patients, were identified from the Cochrane controlled trials register and EMBASE and MEDLINE databases, and subjected to meta-analysis. Remifentanil was associated with a reduction in the time to tracheal extubation after cessation of sedation (weighted-mean-difference -2.04 h (95% CI -0.39 to -3.69 h); p = 0.02). Remifentanil was, however, not associated with a significant reduction in mortality (relative risk 1.01 (95% CI 0.67-1.52); p = 0.96), duration of mechanical ventilation, length of intensive care unit stay, and risk of agitation (relative risk 1.08 (95% CI 0.64-1.82); p = 0.77) when compared to an alternative Sedative or analgesic Agent. The current evidence does not support the routine use of remifentanil as a Sedative Agent in critically ill adult patients.
Ipek Yalcin - One of the best experts on this subject based on the ideXlab platform.
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cortical excitability and activation of trkb signaling during rebound slow oscillations are critical for rapid antidepressant responses
Molecular Neurobiology, 2019Co-Authors: Samuel Kohtala, Wiebke Theilmann, Marko Rosenholm, Leena Penna, Gulsum Karabulut, Salla Uusitalo, Kaija Jarventausta, Arvi Ylihankala, Ipek YalcinAbstract:Rapid antidepressant effects of ketamine become most evident when its psychotomimetic effects subside, but the neurobiological basis of this "lag" remains unclear. Laughing gas (N2O), another NMDA-R (N-methyl-D-aspartate receptor) blocker, has been reported to bring antidepressant effects rapidly upon drug discontinuation. We took advantage of the exceptional pharmacokinetic properties of N2O to investigate EEG (electroencephalogram) alterations and molecular determinants of antidepressant actions during and immediately after NMDA-R blockade. Effects of the drugs on brain activity were investigated in C57BL/6 mice using quantitative EEG recordings. Western blot and qPCR were used for molecular analyses. Learned helplessness (LH) was used to assess antidepressant-like behavior. Immediate-early genes (e.g., bdnf) and phosphorylation of mitogen-activated protein kinase-markers of neuronal excitability-were upregulated during N2O exposure. Notably, phosphorylation of BDNF receptor TrkB and GSK3β (glycogen synthase kinase 3β) became regulated only gradually upon N2O discontinuation, during a brain state dominated by slow EEG activity. Subanesthetic ketamine and flurothyl-induced convulsions (reminiscent of electroconvulsive therapy) also evoked slow oscillations when their acute pharmacological effects subsided. The correlation between ongoing slow EEG oscillations and TrkB-GSK3β signaling was further strengthened utilizing medetomidine, a hypnotic-Sedative Agent that facilitates slow oscillations directly through the activation of α2-adrenergic autoreceptors. Medetomidine did not, however, facilitate markers of neuronal excitability or produce antidepressant-like behavioral changes in LH. Our results support a hypothesis that transient cortical excitability and the subsequent regulation of TrkB and GSK3β signaling during homeostatic emergence of slow oscillations are critical components for rapid antidepressant responses.
Gulsum Karabulut - One of the best experts on this subject based on the ideXlab platform.
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cortical excitability and activation of trkb signaling during rebound slow oscillations are critical for rapid antidepressant responses
Molecular Neurobiology, 2019Co-Authors: Samuel Kohtala, Wiebke Theilmann, Marko Rosenholm, Leena Penna, Gulsum Karabulut, Salla Uusitalo, Kaija Jarventausta, Arvi Ylihankala, Ipek YalcinAbstract:Rapid antidepressant effects of ketamine become most evident when its psychotomimetic effects subside, but the neurobiological basis of this "lag" remains unclear. Laughing gas (N2O), another NMDA-R (N-methyl-D-aspartate receptor) blocker, has been reported to bring antidepressant effects rapidly upon drug discontinuation. We took advantage of the exceptional pharmacokinetic properties of N2O to investigate EEG (electroencephalogram) alterations and molecular determinants of antidepressant actions during and immediately after NMDA-R blockade. Effects of the drugs on brain activity were investigated in C57BL/6 mice using quantitative EEG recordings. Western blot and qPCR were used for molecular analyses. Learned helplessness (LH) was used to assess antidepressant-like behavior. Immediate-early genes (e.g., bdnf) and phosphorylation of mitogen-activated protein kinase-markers of neuronal excitability-were upregulated during N2O exposure. Notably, phosphorylation of BDNF receptor TrkB and GSK3β (glycogen synthase kinase 3β) became regulated only gradually upon N2O discontinuation, during a brain state dominated by slow EEG activity. Subanesthetic ketamine and flurothyl-induced convulsions (reminiscent of electroconvulsive therapy) also evoked slow oscillations when their acute pharmacological effects subsided. The correlation between ongoing slow EEG oscillations and TrkB-GSK3β signaling was further strengthened utilizing medetomidine, a hypnotic-Sedative Agent that facilitates slow oscillations directly through the activation of α2-adrenergic autoreceptors. Medetomidine did not, however, facilitate markers of neuronal excitability or produce antidepressant-like behavioral changes in LH. Our results support a hypothesis that transient cortical excitability and the subsequent regulation of TrkB and GSK3β signaling during homeostatic emergence of slow oscillations are critical components for rapid antidepressant responses.
Feline F J A Ter Bruggen - One of the best experts on this subject based on the ideXlab platform.
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dexmedetomidine vs propofol as sedation for implantation of neurostimulators a single center single blinded randomized controlled trial
Acta Anaesthesiologica Scandinavica, 2019Co-Authors: Feline F J A Ter Bruggen, Charlotte Ceuppens, Leo Leliveld, Dirk L. Stronks, Frank J. P. M. HuygenAbstract:Background: During the lead implantation of most spinal cord neurostimulators, the patient has to be comfortable and without pain. However, the patient is expected to provide feedback during electrical mapping. Titrating Sedatives and analgesics for this double goal can be challenging. In comparison with our standard Sedative Agent propofol, the pharmacological profile of dexmedetomidine is more conducive to produce arousable sedation. The latter, however, is associated with hemodynamic side effects. We investigated whether dexmedetomidine is preferable over propofol during neurostimulator implantation. Methods: This single-center single-blinded randomized controlled trial included 72 patients with an indication for a neurostimulator, randomized to sedation with either propofol (0.5 mg/kg for 10 minutes, followed by 2.0 mg/kg/h) or dexmedetomidine (1 μg/kg for 10 minutes, followed by 0.6 μg/kg/h). The primary outcome was patient satisfaction with the sedation. The secondary outcomes were patient's and operator's comfort, number of titration adjustments, standard intraoperative hemodynamic and respiratory parameters and side effects. Results: Data of 69 patients (dexmedetomidine n = 35; propofol n = 34) were analyzed. Those receiving dexmedetomidine were more satisfied with the sedation than those receiving propofol; i.e. with sedation delivery (median 100.0 vs 83.3, P <.01), procedural recall (median 95.8 vs 83.3, P =.03), and sedation side effects (median 90.0 vs 83.3, P =.01). Fewer changes in the dexmedetomidine titration were necessary to maintain arousable sedation. Over time, mean arterial pressure and heart rate were significantly lower in the dexmedetomidine group. Hemodynamic side effects were comparable across groups. Conclusions: Dexmedetomidine sedation resulted in higher patient satisfaction and allowed for better arousable sedation than sedation with propofol. Although differences in hemodynamic parameters were found between the groups, these differences were not regarded as clinically relevant.
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efficacy of dexmedetomidine as a sole Sedative Agent in small diagnostic and therapeutic procedures a systematic review
Pain Practice, 2017Co-Authors: Feline F J A Ter Bruggen, Dirk L. Stronks, Ismail Eralp, Chris K Jansen, F HuygenAbstract:Dexmedetomidine is an upcoming Agent with Sedative, anxiolytic, and analgesic properties. This review summarizes empirical evidence for the efficacy of dexmedetomidine as a sole Sedative Agent, and its effectiveness for small diagnostic and therapeutic procedure, in comparison with other frequently used Sedatives. All randomized controlled trials on the effect of dexmedetomidine were reviewed. Pain level, patient satisfaction, operator satisfaction, procedure duration, recovery time, and hemodynamic and respiratory characteristics were examined. A total of 1993 patients (1,621 adults; 372 children) from 35 studies were included. In the adult studies, dexmedetomidine yielded significantly lower pain levels compared to the other Sedatives (in 31.25% of the included studies) and significantly more patient satisfaction (68.2%). In studies on children, more favorable results concerning respiratory safety and the level of adequate sedation were found compared to the control Sedatives. Implications for future studies are discussed.
Samuel Kohtala - One of the best experts on this subject based on the ideXlab platform.
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cortical excitability and activation of trkb signaling during rebound slow oscillations are critical for rapid antidepressant responses
Molecular Neurobiology, 2019Co-Authors: Samuel Kohtala, Wiebke Theilmann, Marko Rosenholm, Leena Penna, Gulsum Karabulut, Salla Uusitalo, Kaija Jarventausta, Arvi Ylihankala, Ipek YalcinAbstract:Rapid antidepressant effects of ketamine become most evident when its psychotomimetic effects subside, but the neurobiological basis of this "lag" remains unclear. Laughing gas (N2O), another NMDA-R (N-methyl-D-aspartate receptor) blocker, has been reported to bring antidepressant effects rapidly upon drug discontinuation. We took advantage of the exceptional pharmacokinetic properties of N2O to investigate EEG (electroencephalogram) alterations and molecular determinants of antidepressant actions during and immediately after NMDA-R blockade. Effects of the drugs on brain activity were investigated in C57BL/6 mice using quantitative EEG recordings. Western blot and qPCR were used for molecular analyses. Learned helplessness (LH) was used to assess antidepressant-like behavior. Immediate-early genes (e.g., bdnf) and phosphorylation of mitogen-activated protein kinase-markers of neuronal excitability-were upregulated during N2O exposure. Notably, phosphorylation of BDNF receptor TrkB and GSK3β (glycogen synthase kinase 3β) became regulated only gradually upon N2O discontinuation, during a brain state dominated by slow EEG activity. Subanesthetic ketamine and flurothyl-induced convulsions (reminiscent of electroconvulsive therapy) also evoked slow oscillations when their acute pharmacological effects subsided. The correlation between ongoing slow EEG oscillations and TrkB-GSK3β signaling was further strengthened utilizing medetomidine, a hypnotic-Sedative Agent that facilitates slow oscillations directly through the activation of α2-adrenergic autoreceptors. Medetomidine did not, however, facilitate markers of neuronal excitability or produce antidepressant-like behavioral changes in LH. Our results support a hypothesis that transient cortical excitability and the subsequent regulation of TrkB and GSK3β signaling during homeostatic emergence of slow oscillations are critical components for rapid antidepressant responses.