Anesthesiology
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Retropharyngeal hematoma (RPH) is rare; however, it causes airway obstruction and can be fatal. Stellate ganglion block (SGB) can cause RPH. The authors analyzed reports of patients with RPH after SGB to clarify the initial symptoms and signs, and the urgency of airway management. ⋯ RPH after SGB necessitates emergency airway management. Because airway obstruction cannot be predicted by the initial symptoms or signs, emergency airway management tools should be at hand, and the patency of the airway should be continuously evaluated after onset of RPH after SGB.
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The volatile anesthetic isoflurane induces hypoxia inducible factor (HIF)-1-responsive genes heme oxygenase 1, inducible nitric oxide synthase, and vascular endothelial growth factor (VEGF) expression. Little is known about the extent to which induction of HIF-1alpha is affected by isoflurane. ⋯ Isoflurane can up-regulate HIF-1alpha and enhance HIF-1-responsive genes heme oxygenase 1, inducible nitric oxide synthase, and VEGF mRNA expression in Hep3B cells. The induction of HIF-1alpha by isoflurane does not involve protein degradation but depends on translation pathway.
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L-Arginine transport mediated by type 2 cationic amino acid transporter (CAT-2) is one crucial mechanism that regulates nitric oxide production mediated by inducible nitric oxide synthase. Heme oxygenase (HO)-1 induction has been reported to significantly attenuate inducible nitric oxide synthase expression and nitric oxide production. The authors sought to explore the effects of HO-1 induction on CAT-2 expression and L-arginine transport. The effects of HO-1 induction on nuclear factor E2-related factor 2 (Nrf2) and nuclear factor kappaB (NF-kappaB) were also investigated. ⋯ HO-1 induction significantly inhibited CAT-2 expression and L-arginine transport in lipopolysaccharide-stimulated macrophages, possibly through mechanisms involved activation of Nrf2 and inhibition of NF-kappaB. In addition, carbon monoxide mediated, at least in part, the effects of HO-1 induction on CAT-2 expression and L-arginine transport.
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Intravenous anesthetics cause amnesia, but the underlying molecular mechanisms are poorly understood. Recent studies reveal a significant role of extracellular signal-regulated protein kinases (ERKs) in controlling synaptic plasticity and memory formation. As a major synapse-to-nucleus superhighway, ERK transmits N-methyl-D-aspartate (NMDA) receptor signals to inducible transcriptional events essential for NMDA receptor-dependent forms of synaptic plasticity and memory. This study investigated the role of the widely used intravenous anesthetic propofol in regulating NMDA receptor-dependent ERK phosphorylation. ⋯ These results suggest that propofol possesses the ability to inhibit NMDA receptor activation of the ERK pathway and subsequent transcriptional activities in hippocampal neurons. These findings indicate a new avenue to explore a transcription-dependent mechanism that may underlie anesthetic interference with synaptic plasticity related to amnesic properties of intravenous anesthetics.
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The authors used the American Society of Anesthesiologists Closed Claims Project database to determine changes in the proportion of claims for death or permanent brain damage over a 26-yr period and to identify factors associated with the observed changes. ⋯ The significant decrease in the proportion of claims for death or permanent brain damage from 1975 through 2000 seems to be unrelated to a marked increase in the proportion of claims where pulse oximetry and end-tidal carbon dioxide monitoring were used. After the introduction and use of these monitors, there was a significant reduction in the proportion of respiratory and an increase in the proportion of cardiovascular damaging events responsible for death or permanent brain damage.