Masui. The Japanese journal of anesthesiology
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A 69-year-old man with normal renal function underwent resection of a parotid tumor under general anesthesia. For tracheal intubation, rocuronium 0.6 mg x kg(-1) was administered, and for facial nerve stimulation, sugammadex 2 mg x kg(-1) was administered immediately after intubation. The operation time was 3 h. ⋯ The times for both maximal suppression and recovery are similar to those when the same dose of rocuronium was used without sugammadex. The half-life of sugammadex is about 2 h. From the observations in this case, we think that after the completion of approximately 3 half-lives, a normal dose of rocuronium can produce the desired effect without the influence of residual sugammadex present in the plasma.
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Recent advancement in functional brain imaging techniques has revealed much of the global effects of general anesthetics on the human brain. General anesthetics preferentially suppress specific brain areas including the parietal association cortex and the thalamus, part of which appears to mirror the default mode network. ⋯ Midazolam-induced loss of consciousness is associated with remarkable suppression of cortico-cortical propagation of evoked currents. Overall, those results prompt us to hypothesize that general anesthetics induce loss of consciousness by disrupting the integrative properties of the cerebral cortex.
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Recently, almost all kinds of general anesthetics currently used in human clinical anesthesia, have been shown to exert neurodegenerative effects such as apoptosis of neuronal cells during the rapid synaptogenesis of immature mammalian brains, and later neurocognitive impairment. There are several drugs or strategies to reduce this phenomenon such as alpha(2) agonist, xenon, melatonin, lithium, hypothermia and erythropoietin, but their safety and efficacy should be investigated much further. ⋯ Larger-sized prospective randomized studies in human such as SAFEKIDS (http://www.iars.org/safekids/) to ascertain if current clinical practice of general anesthesia impairs neurocognitive development of human neonates and infants, are expected. They will also clarify what kind of anesthetics and anesthetic strategies may be the risk factors of neurocognitive impairment in human neonates and infants.
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Although general anesthetics were first used more than 160 years ago, their mechanisms have remained mysterious. During the past decade, significant progress in our understanding of general anesthetic action at the cellular and network system levels has been made. Our recent work demonstrates (a) that intravenous anesthetics, but not volatile agents, enhance the discharge of GABA from presynaptic terminals, (b) that intravenous anesthetics produce frequency-dependent modification (FDM) of anesthesia, and (c) that FDM is responsible for the unsuccessful immobilization or hypnosis during intravenous anesthesia. In addition, we review the development of hypothesis for anesthetic action, non-specific versus specific action, cutoff phenomenon in n-alcohols, and anesthesiological approach to consciousness.
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It is widely known that electroencephalogram (EEG) shows dramatic changes with increase of the concentration of anesthetic. It is considered that volatile anesthetics (i. e. isoflurane, sevoflurane), barbiturates, propofol show anesthetic effect by potentiating GABAA receptor. Changing patterns of EEG by these anesthetics are quite similar. ⋯ However this is not always the required condition for adequate anesthesia, because alpha power never becomes larger in some patients even when the anesthetic level was judged as adequate by concentration dependent changing patterns of EEG. As EEG changes in relation to the concentration of anesthetic, it seems to be correlated with the level of consciousness. But EEG patterns during anesthesia are mainly determined by the condition of thalamic neurons, and it would merely indicate the level of hypnosis indirectly.