Anesthesiology
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It is not known whether thromboxane A2 impairs adenosine triphosphate (ATP)-sensitive K channel function via increased production of superoxide in blood vessels and whether propofol as a nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitor restores this modification. ⋯ Thromboxane receptor activation induces vascular oxidative stress via NADPH oxidase, resulting in the impairment of ATP-sensitive K channel function. Propofol reduces this stress via inhibition of a NADPH oxidase subunit p47phox and, therefore, restores ATP-sensitive K channel function.
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In a patient whose airway is likely to become obstructed upon loss of consciousness, anesthesia may be induced using an inhaled vapor. If the airway occludes during such an inhalational induction, the speed of patient awakening is related to the rate at which anesthetic gas redistributes away from lung and brain to other body compartments. To determine whether redistribution occurs more rapidly with a more blood-soluble or a less blood-soluble agent, the authors used subanesthetic concentrations of halothane and sevoflurane to simulate inhalational induction and airway obstruction in eight healthy human volunteers. ⋯ During simulated airway occlusion in healthy volunteers, the end-tidal concentration of halothane falls more rapidly than that of sevoflurane. Halothane may therefore lead to more rapid awakening, compared with sevoflurane, should the airway obstruct during an inhalational induction of anesthesia.
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Numerous electronic devices have been introduced into operating rooms. Although little is known about the relationship between exposure to electromagnetic fields and health hazards, several studies have demonstrated causal relationships between electromagnetic fields exposure and various symptoms, cancers, and other diseases. ⋯ The authors' results indicate that anesthesiologists in operating rooms are exposed to extremely low-frequency electromagnetic field levels that exceed magnetic field intensity of 2 mG recommended by the Swedish Board for Technical Accreditation for production by computer monitors and detected 30 cm from them. It currently is not clear if this exposure has health effects on anesthesiologists and other operating room personnel.
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The cellular mechanisms of neuropathic pain are inadequately understood. Previous investigations have revealed disrupted Ca signaling in primary sensory neurons after injury. The authors examined the effect of injury on intracellular Ca stores of the endoplasmic reticulum, which critically regulate the Ca signal and neuronal function. ⋯ Painful nerve injury leads to diminished releasable endoplasmic reticulum Ca stores and a reduced luminal Ca concentration. Depletion of Ca stores may contribute to the pathogenesis of neuropathic pain.
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Preconditioning neurons with noninjurious hypoxia (hypoxic preconditioning, HPC) or the anesthetic isoflurane (APC) induces tolerance of severe ischemic stress. The mechanisms of both types of preconditioning in the hippocampus require moderate increases in intracellular Ca and activation of protein kinase signaling. The authors hypothesized that the expression of signal transduction genes would be similar after APC and HPC. ⋯ Despite sharing similar upstream signaling and neuroprotective outcomes, the genomic response to APC and HPC is different. Increased expression of antiapoptosis genes after HPC and cell development genes after APC has implications both for neuroprotection and long-term effects of anesthetics.