Anesthesiology
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Comparative Study
In vivo imaging of nitrous oxide-induced changes in cerebral activation during noxious heat stimuli.
Although previous studies have provided some insight into the pharmacologic aspects of nitrous oxide analgesia, the neural circuits mediating its antinociceptive effect remain relatively unexplored. Position emission tomography was used in nine volunteers to identify the loci of nitrous oxide-modulated cerebral responses to a peripheral noxious stimulus. ⋯ Nitrous oxide, at 20% concentration, appears to modulate pain processing in the brain's medial pain system, and also activates the infralimbic and orbitofrontal cortices. The potential contribution of the affected brain areas to nitrous oxide analgesia is discussed.
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Children with spina bifida are at greater risk for latex and ethylene oxide sensitization. The authors' aim in this study was to evaluate the role of previous surgical procedures in the development of sensitization to latex and ethylene oxide. ⋯ Results suggest that it is the number of surgical procedures rather than spina bifida per se that is related to sensitization to latex.
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The authors report on the appearance of misleading square wave "phantom" capnograph tracings for approximately 3 min after disconnection from the Siemens Servo 900c ventilator. A series of experiments are described to examine the mechanism of this phenomenon. ⋯ After accidental disconnection of the patient from the breathing system, or after accidental extubation of the trachea, the "phantom" capnograph is likely to confuse even an experienced anesthesiologist into the mistaken belief that his rapidly deteriorating patient is being ventilated adequately. Several potential mechanisms to eliminate this phenomenon are outlined, including the avoidance of zero positive end-expiratory pressure. "Phantom" capnography provides an illustration of the dangers of using monitoring techniques, however reliable, as a substitute for vigilant clinical observation.
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The influence of anesthetic agents on the infarction process in the ischemic myocardium is unclear. This study evaluated the effects of three intravenous and three inhalational anesthetic agents on myocardial infarction within a quantified ischemic risk zone in rabbit hearts subjected to a standardized regional ischemia-reperfusion insult. ⋯ The volatile anesthetics tested protected the ischemic rabbit heart from infarction, in contrast to the three intravenous agents tested. Protection was independent of the hypotensive effect of the inhalational agents because halothane also protected isolated hearts, in which changing vascular tone is not an issue and coronary perfusion pressure is constant. Cardioprotection by volatile anesthetics depended on both adenosine receptors and protein kinase C, and thus is similar to the mechanism of protection seen with ischemic preconditioning.
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Although the anesthetic effects of the intravenous anesthetic agent propofol have been studied in the living human brain using brain imaging technology, the nature of the anesthetic state evident in the human brain during inhalational anesthesia remains unknown. To examine this issue, the authors studied the effects of isoflurane anesthesia on human cerebral glucose metabolism using positron emission tomography (PET). ⋯ These data clarify that the anesthetic state evident in the living human brain during unresponsiveness induced with isoflurane is associated with a global, fairly uniform, whole-brain glucose metabolic reduction of 46 +/- 11%.