Journal: Anesthesiology

Abbreviation

Anesthesiology

Publisher

Lippincott Williams & Wilkins

Journal Volumes

ISSN

0003-3022
1528-1175

Description

Filters

2004 - 200972020 - 20221
Reset filters

Search Results

Publications 1 - 8 of 8
  • Simulators in Critical Care and Beyond
    Item type: Journal Article
    Manser, Tanja (2005)
    Anesthesiology
  • Isoflurane Postconditioning Prevents Opening of the Mitochondrial Permeability Transition Pore through Inhibition of Glycogen Synthase Kinase 3β
    Item type: Journal Article
    Feng, Jianhua; Lucchinetti, Eliana; Ahuja, Preeti; et al. (2005)
    Anesthesiology
  • The well-being model
    Item type: Conference Paper
    Zanderigo, Eleonora; Sartori, Valentina; Sveticic, Gorazd; et al. (2006)
    Anesthesiology
  • The Well-being Model
    Item type: Conference Paper
    Zanderigo, Eleonora; Sartori, Valentina; Sveticic, Gorazd; et al. (2006)
    Anesthesiology
  • A new closed-loop control sysyem for isoflurane using Bispectral Index outperforms manual control
    Item type: Journal Article
    Locher, Stephan; Stadler, Konrad S.; Boehlen, Thomas; et al. (2004)
    Anesthesiology
  • Combinations of bupivacaine, fentanyl, and clonidine for lumbar epidural postoperative analgesia
    Item type: Journal Article
    Sveticic, Gorazd; Gentilini, Andrea; Eichenberger, Urs; et al. (2004)
    Anesthesiology
  • Midazolam at Low Nanomolar Concentrations Affects Long-term Potentiation and Synaptic Transmission Predominantly via the alpha(1)-gamma-Aminobutyric Acid Type A Receptor Subunit in Mice
    Item type: Journal Article
    Puig-Bosch, Xenia; Bieletzki, Stefan; Zeilhofer, Hanns U.; et al. (2022)
    Anesthesiology
    Background Midazolam amplifies synaptic inhibition via different γ-aminobutyric acid type A (GABAA) receptor subtypes defined by the presence of α1-, α2-, α3-, or α5-subunits in the channel complex. Midazolam blocks long-term potentiation and produces postoperative amnesia. The aims of this study were to identify the GABAA receptor subtypes targeted by midazolam responsible for affecting CA1 long-term potentiation and synaptic inhibition in neocortical neurons. Methods The effects of midazolam on hippocampal CA1 long-term potentiation were studied in acutely prepared brain slices of male and female mice. Positive allosteric modulation on GABAA receptor–mediated miniature inhibitory postsynaptic currents was investigated in organotypic slice cultures of the mouse neocortex. In both experiments, wild-type mice and GABAA receptor knock-in mouse lines were compared in which α1-, α5-, α1/2/3-, α1/3/5- and α2/3/5-GABAA receptor subtypes had been rendered benzodiazepine-insensitive. Results Midazolam (10 nM) completely blocked long-term potentiation (mean ± SD, midazolam, 98 ± 11%, n = 14/8 slices/mice vs. control 156 ± 19%, n = 20/12; P < 0.001). Experiments in slices of α1-, α5-, α1/2/3-, α1/3/5-, and α2/3/5–knock-in mice revealed a dominant role for the α1-GABAA receptor subtype in the long-term potentiation suppressing effect. In slices from wild-type mice, midazolam increased (mean ± SD) charge transfer of miniature synaptic events concentration-dependently (50 nM: 172 ± 71% [n = 10/6] vs. 500 nM: 236 ± 54% [n = 6/6]; P = 0.041). In α2/3/5–knock-in mice, charge transfer of miniature synaptic events did not further enhance when applying 500 nM midazolam (50 nM: 171 ± 62% [n = 8/6] vs. 500 nM: 175 ± 62% [n = 6/6]; P = 0.454), indicating two different binding affinities for midazolam to α2/3/5- and α1-subunits. Conclusions These results demonstrate a predominant role of α1-GABAA receptors in the actions of midazolam at low nanomolar concentrations. At higher concentrations, midazolam also enhances other GABAA receptor subtypes. α1-GABAA receptors may already contribute at sedative doses to the phenomenon of postoperative amnesia that has been reported after midazolam administration.
  • Infarct-remodeled myocardium is receptive to protection by isoflurane postconditioning
    Item type: Journal Article
    Feng, Jianhua; Fischer, Gregor; Lucchinetti, Eliana; et al. (2006)
    Anesthesiology
Publications 1 - 8 of 8