2014
DOI: 10.1016/j.anclin.2013.10.003
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Anesthetic Neurotoxicity

Abstract: All routinely utilized sedatives and anesthetics have been found neurotoxic in a wide variety of animal species, including non-human primates. Neurotoxic effects observed in animals include histologic evidence for apoptotic neuronal cell death and subsequent learning and memory impairment. Several cohort studies in neonates with significant comorbidities requiring surgical procedures early in life have also demonstrated abnormal neurodevelopmental outcomes. This article provides an overview of the currently av… Show more

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Cited by 91 publications
(60 citation statements)
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“…[16,21,25] The mechanism by which local anesthetics trigger its neurotoxic effects involves induction of apoptosis, which starts with the increased conductance of the calcium channels, with an increase of the intracellular concentration of this, production of reactive oxygen species and release of cytochrome c into the cytosol, culminating with the induction of caspases formation, decrease of the expression of anti-apoptotic proteins (Bcl-2) and increased expression of pro-apoptotic proteins (BAX), inducing acceleration of programmed cell death. [5,17,26] Anesthesia and surgery on their own induce the release of cytokines, especially IL-1β and IL-6, as well as the factor of tumor necrosis) TNF-α, triggering a proinflammatory state that contributes to postoperative cognitive disorders. Lidocaine administered systemically has anti-inflammatory properties and may prove to be an adjuvant to mitigate these deleterious effects.…”
Section: Discussionmentioning
confidence: 99%
“…[16,21,25] The mechanism by which local anesthetics trigger its neurotoxic effects involves induction of apoptosis, which starts with the increased conductance of the calcium channels, with an increase of the intracellular concentration of this, production of reactive oxygen species and release of cytochrome c into the cytosol, culminating with the induction of caspases formation, decrease of the expression of anti-apoptotic proteins (Bcl-2) and increased expression of pro-apoptotic proteins (BAX), inducing acceleration of programmed cell death. [5,17,26] Anesthesia and surgery on their own induce the release of cytokines, especially IL-1β and IL-6, as well as the factor of tumor necrosis) TNF-α, triggering a proinflammatory state that contributes to postoperative cognitive disorders. Lidocaine administered systemically has anti-inflammatory properties and may prove to be an adjuvant to mitigate these deleterious effects.…”
Section: Discussionmentioning
confidence: 99%
“…However, recently observed subsequent behavioral abnormalities and diminished academic performance have raised significant concerns regarding the safe use of anesthetics in children. 1 The phenomenon's etiology remains under investigation; however, animal studies in a variety of species have demonstrated widespread neuronal cell death, permanent neuronal deletion, alterations in dendritic architecture, or long-term learning and memory impairment after exposure to all commonly used anesthetics (most recently reviewed in Lin et al 2 ). Because anesthetics are potent modulators of excitatory and inhibitory neurotransmission, the assertion that anesthetic exposure may interfere with proper development of the immature brain is not entirely implausible.…”
Section: What This Study Addsmentioning
confidence: 99%
“…В процессе развития ише-мии мозговой ткани большое значение имеют ток-сическое воздействие на клетку избыточного коли-чества накопившихся возбуждающих аминокислот (эксайтотоксичность), лавинообразное поступление в клетки ионов кальция, распад клеточных мембран, накопление свободных радикалов и продуктов пере-кисного окисления липидов. При этом происходит за-пуск каскада патохимических реакций апоптогенной гибели нейронов, что влечет за собой развитие интра-и постоперационных осложнений, диапазон которых при общем обезболивании весьма широк [1,2,5,6].…”
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