Anesthesiology
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Letter Clinical Trial
Jet venturi ventilation via the Bullard laryngoscope.
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Typically, core temperature rapidly decreases after induction of anesthesia, but reaches a stable plateau after several hours. This plateau typically occurs in conjunction with the onset of thermoregulatory vasoconstriction. Decreased heat loss, caused by vasoconstriction, may not be sufficient to establish thermal steady state without a concomitant increase in heat production. Accordingly, the authors tested the hypothesis that nonshivering thermogenesis contributes to thermal steady state during anesthesia. Rewarming from hypothermia is often associated with an afterdrop (a further reduction in core temperature, despite cutaneous warming). Because total body heat content increases during cutaneous warming, heat storage during afterdrop must reflect increased temperature and heat content of the peripheral tissue mass. Thermal balance was measured during rewarming to estimate the thermal capacity of the peripheral tissues. ⋯ The authors concluded that nonshivering thermogenesis is not an important thermoregulatory response in adults anesthetized with isoflurane. Afterdrop and delayed core temperature recovery during rewarming reflect the large heat storage capacity of peripheral tissues.
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The minimum alveolar concentration (MAC) of desflurane/oxygen is 7.25% in the 18-30-yr age group, and 6.0% in the 31-65-yr age group. The addition of 60% N2O reduces MAC to 4.0 and 2.83%, respectively. Because MAC of other inhaled anesthetics is less than that for younger adults, we determined MAC of desflurane in adults aged 65 yr and older. ⋯ In the geriatric patient, MAC of desflurane, with or without nitrous oxide, is less than that reported in patients aged 18-65 yr. This is in agreement with results with all other inhalation agents.
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The molecular mechanism of propofol anesthesia has been related to facilitation of the inhibitory neurotransmission mediated by gamma-aminobutyric acid (GABA). In the current study, the authors examined the direct actions of propofol on the acutely dissociated mammalian central neurons. ⋯ Propofol at clinically relevant concentrations directly activates the GABAA receptor-chloride ionophore complex in the mammalian central neurons and, hence, increases the chloride conductance, which may contribute to anesthesia produced by the agent. The desensitization of the GABAA receptor in the presence of high concentrations of propofol may result in a suppression of the GABAA inhibitory system.