Anesthesiology
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Increasing evidence supports a role for brain reward circuitry in modulating arousal along with emergence from anesthesia. Emergence remains an important frontier for investigation, since no drug exists in clinical practice to initiate rapid and smooth emergence. ⋯ Then there is a description of modern systems neuroscience approaches to neural circuit investigations that will help span the large gap between preclinical and clinical investigation with the shared aim of developing therapies to promote rapid emergence without agitation or delirium. This article proposes that neuroscientists include models of whole-brain network activity in future studies to inform the translational value of preclinical investigations and foster productive dialogues with clinician anesthesiologists.
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Noncardiac surgery conveys a substantial risk of secondary organ dysfunction and injury. Neurocognitive dysfunction and covert stroke are emerging as major forms of perioperative organ dysfunction, but a better understanding of perioperative neurobiology is required to identify effective treatment strategies. ⋯ Translation of these imaging methods into the perioperative setting has highlighted several potential avenues to optimize tissue perfusion and deliver neuroprotection. This review introduces the methods, metrics, and evidence underlying emerging optical and magnetic resonance neuroimaging methods and discusses their potential experimental and clinical utility in the setting of noncardiac surgery.
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Residual neuromuscular blockade can be avoided with quantitative neuromuscular monitoring. The authors embarked on a professional practice initiative to attain documented train-of-four ratios greater than or equal to 0.90 in all patients for improved patient outcomes through reducing residual paralysis. ⋯ In this professional practice initiative, documentation of train-of-four ratios greater than or equal to 0.90 occurred for 93% of patients in a busy clinical practice. Return-of-strength documentation is an intermediate outcome, and only one of many factors contributing to patient outcomes.
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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. ⋯ 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.