Anesthesiology
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Patients with obstructive sleep apnea are at risk for perioperative morbidity. The authors used a screening prediction model for obstructive sleep apnea to generate a sleep apnea clinical score (SACS) that identified patients at high or low risk for obstructive sleep apnea. This was combined with postanesthesia care unit (PACU) monitoring with the aim of identifying patients at high risk of postoperative oxygen desaturation and respiratory complications. ⋯ Combination of an obstructive sleep apnea screening tool preoperatively (SACS) and recurrent PACU respiratory events was associated with a higher oxygen desaturation index and postoperative respiratory complications. A two-phase process to identify patients at higher risk for perioperative respiratory desaturations and complications may be useful to stratify and manage surgical patients postoperatively.
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Postoperative delirium is associated with increased morbidity and mortality. Preexisting cognitive impairment and depression have been frequently cited as important risk factors for this complication. This prospective cohort study was designed to determine whether individuals who perform poorly on preoperative cognitive tests and/or exhibited depressive symptoms would be at high risk for the development of postoperative delirium. ⋯ Low preoperative executive scores and depressive symptoms independently predict postoperative delirium in older individuals. A rapid, simple test combination including tests of executive function and depression could improve physicians' ability to recognize patients who might benefit from a perioperative intervention strategy to prevent postoperative delirium.
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Exposure to anesthetics during synaptogenesis results in apoptosis and subsequent cognitive dysfunction in adulthood. Probrain-derived neurotrophic factor (proBDNF) is involved in synaptogenesis and can induce neuronal apoptosis via p75 neurotrophic receptors (p75). proBDNF is cleaved into mature BDNF (mBDNF) by plasmin, a protease converted from plasminogen by tissue plasminogen activator (tPA) that is released with neuronal activity; mBDNF supports survival and stabilizes synapses through tropomyosin receptor kinase B. The authors hypothesized that anesthetics suppress tPA release from neurons, enhance p75 signaling, and reduce synapses, resulting in apoptosis. ⋯ tPA, plasmin, or p75 inhibition blocked isoflurane-mediated reduction in dendritic filopodial spines and neuronal apoptosis in vitro. Isoflurane reduced synapses and enhanced Cl-Csp3 in the hippocampus of PND5-7 mice, the latter effect being mitigated by p75 inhibition in vivo. These data support the hypothesis that isoflurane neurotoxicity in the developing rodent brain is mediated by reduced synaptic tPA release and enhanced proBDNF/p75-mediated apoptosis.
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Emerging evidence indicates that an endogenous autocrine/paracrine system involving gamma-aminobutyric acid (GABA) is present in airways. GABAA channels, GABAB receptors, and the enzyme that synthesizes GABA have been identified in airway epithelium and smooth muscle. However, the endogenous ligand itself, GABA, has not been measured in airway tissues. The authors sought to demonstrate that GABA is released in response to contractile agonists and tonically contributes a prorelaxant component to contracted airway smooth muscle. ⋯ These studies demonstrate that GABA is endogenously present and increases after contractile stimuli in guinea pig upper airways and that endogenous GABA contributes a tonic prorelaxant component in the maintenance of airway smooth muscle tone.
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Anesthetic agents cause cell death in the developing rodent brain and long-term, mostly hippocampal-dependent, neurocognitive dysfunction. However, a causal link between these findings has not been shown. Postnatal hippocampal neurogenesis affects hippocampal function into adulthood; therefore, the authors tested the hypothesis that isoflurane affects long-term neurocognitive function via an effect on dentate gyrus neurogenesis. ⋯ The authors conclude that isoflurane differentially affects both neurogenesis and long-term neurocognitive function in P60 and P7 rats. Neurogenesis might mediate the long-term neurocognitive outcome after isoflurane at different ages.