Anesthesiology
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Randomized Controlled Trial Clinical Trial
Duration of anesthesia before muscle relaxant injection influences level of paralysis.
Dosage guidelines for muscle relaxants are based on dose-response studies, normally performed after several minutes of stable nitrous oxide (N O)-opioid anesthesia. However, relaxants are used immediately after induction of anesthesia. The study was designed to determine the influence of the duration of anesthesia and N O on the onset time at the adductor pollicis (AP) and the corrugator supercilii (CS) muscles of maximum neuromuscular blockade after mivacurium. ⋯ Duration of anesthesia and N O before mivacurium injection affect intensity of neuromuscular blockade but not onset time. Neuromuscular blockade obtained at the AP after several minutes of stable anesthesia with N O is greater than immediately after induction. This explains in part the discrepancy between the measured ED and the intubating dose.
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The most appropriate method of determining positive end-expiratory pressure (PEEP) level during a lung protective ventilatory strategy has not been established. ⋯ Although generating higher plateau pressures, PEEP levels based on pressure-volume curve analysis were more effective in maintaining gas exchange and minimizing injury than PEEP based on adequate oxygenation. PEEP at 2 cm H(2)O above the lower inflection point was most effective.
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During severe isovolemic hemodilution, determination of critical hematocrit levels for the microvascular oxygenation of different organs might provide more insight into the effect of the redistribution of blood flow and oxygen delivery on the oxygenation of different organs. The effect of an increased amount of dissolved oxygen on tissue oxygenation during severely decreased hematocrit levels is not clear. ⋯ During isovolemic hemodilution, the diminished oxygen supply was redistributed in favor of organs with a lower capacity to increase oxygen extraction. It is hypothesized that redirection of the oxygen supply within the intestines resulted in the preservation of oxygen consumption and mucosal muPo(2) compared with serosal muPo(2).
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Bupivacaine produces skeletal muscle damage in clinical concentrations. It has been suggested that this may be caused by an increased intracellular level of [Ca2+]. Therefore, the aim of this study was to investigate direct intracellular effects of bupivacaine on Ca2+ release from the sarcoplasmic reticulum (SR), on Ca2+ uptake into the SR, and on Ca2+ sensitivity of the contractile proteins. ⋯ These data reveal that bupivacaine does not only induce Ca2+ release from the SR, but also inhibits Ca2+ uptake by the SR, which is mainly regulated by SR Ca2+ adenosine triphosphatase activity. It also has a Ca2+ -sensitizing effect on the contractile proteins. These mechanisms result in increased intracellular [Ca2+] concentrations and may thus contribute to its pronounced skeletal muscle toxicity.