Anesthesiology
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Randomized Controlled Trial Clinical Trial
Effects of recruitment maneuver on atelectasis in anesthetized children.
General anesthesia is known to promote atelectasis formation. High inspiratory pressures are required to reexpand healthy but collapsed alveoli. However, in the absence of positive end-expiratory pressure (PEEP), reexpanded alveoli collapse again. Using magnetic resonance imaging, the impact of an alveolar recruitment strategy on the amount and distribution of atelectasis was tested. ⋯ Frequency of atelectasis was much less following the alveolar recruitment strategy, compared with children who did not have the maneuver performed. The mere application of 5 cm H2O of CPAP without a prior recruitment did not show the same treatment effect and showed no difference compared to the control group without PEEP.
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Randomized Controlled Trial Clinical Trial
Optimal oxygen concentration during induction of general anesthesia.
The use of 100% oxygen during induction of anesthesia may produce atelectasis. The authors investigated how different oxygen concentrations affect the formation of atelectasis and the fall in arterial oxygen saturation during apnea. ⋯ During routine induction of general anesthesia, 80% oxygen for oxygenation caused minimal atelectasis, but the time margin before unacceptable desaturation occurred was significantly shortened compared with 100% oxygen.
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Because obesity might affect pharmacokinetic parameters, the authors evaluated the accuracy of target-controlled sufentanil infusion in morbidly obese patients using a pharmacokinetic model usually applied to a normal-weight population. ⋯ The pharmacokinetic parameter set derived from a normal-weight population accurately predicted plasma sufentanil concentrations in morbidly obese patients.
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Systemic inflammation may be associated with resistance to nondepolarizing neuromuscular blocking drugs, the mechanisms of which are, however, uncharacterized. The authors therefore investigated the pharmacodynamics of atracurium and its relation to the expression of nicotinic acetylcholine receptors and alpha1 -acid glycoprotein in a rat model of systemic inflammation. ⋯ Resistance to atracurium during corynebacterium parvum-induced systemic inflammation is due to increased drug binding to alpha1 -acid glycoprotein and is unrelated to changes in acetylcholine receptor expression.
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Pathophysiology in the primary sensory neuron may contribute to chronic neuropathic pain. Ca channels play a central role in neuronal processes, and sensory neurons are rich in low-voltage-activated calcium channels (LVACCs). However, the physiologic function of these channels is unknown. Their possible role in rebound burst firing makes them a candidate for increased excitability after neuropathic injury. ⋯ These results suggest that loss of LVACC may contribute to decreased spike frequency adaptation and increased excitability after injury to sensory neurons. Through decreased Ca2+ influx, the cell becomes less stable and more likely to initiate or transmit bursts of action potentials. Consequently, modulation of Ca2+ currents at the dorsal root ganglion may be a potential method of therapeutic intervention.