2020
DOI: 10.1007/s00540-020-02812-9
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General anesthesia affecting on developing brain: evidence from animal to clinical research

Abstract: As the recent update of General anaesthesia compared to spinal anaesthesia (GAS) studies has been published in 2019, together with other clinical evidence, the human studies provided an overwhelming mixed evidence of an association between anaesthesia exposure in early childhood and later neurodevelopment changes in children. Pre-clinical studies in animals provided strong evidence on how anaesthetic and sedative agents (ASAs) causing neurotoxicity in developing brain and deficits in long-term cognitive functi… Show more

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Cited by 48 publications
(37 citation statements)
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“…In 2016, the US Food and Drug Administration issued a safety communication stating that the repeated or prolonged (>3 h) exposure to anesthetics in children younger than 3 years may negatively affect brain development (36,37). The statement was mainly based on in vitro and animal studies, whereas as expected in the absence of a control group, clinical studies seem ambivalent (38).…”
Section: Discussionmentioning
confidence: 99%
“…In 2016, the US Food and Drug Administration issued a safety communication stating that the repeated or prolonged (>3 h) exposure to anesthetics in children younger than 3 years may negatively affect brain development (36,37). The statement was mainly based on in vitro and animal studies, whereas as expected in the absence of a control group, clinical studies seem ambivalent (38).…”
Section: Discussionmentioning
confidence: 99%
“…In 2016, the US Food and Drug Administration published a warning regarding the prolonged (>3 h) or repeated exposure to anesthetics in children younger than 3 years, as it may affect brain development ( 22 , 23 ). This concern was mainly based on animal studies, whereas clinical studies seem ambivalent ( 24 26 ). Emerging clinical studies support a dose-response relationship between general anesthesia exposure and neurotoxicity ( 24 ), suggesting that, in children, a single exposure ( 24 ) and/or exposures up to 1 h ( 25 ) are not associated with detectable risks of long-term consequences.…”
Section: Discussionmentioning
confidence: 99%
“…The intrinsic pathway is initiated in response to signals from within the cell, resulting in a decreasing anti-apoptotic (such as BCL-2, MCL1, BCL-XL) and pro-apoptotic (BAX/BAK) ratio, which induces mitochondrial outer membrane permeabilization (MOMP). MOMP promoted cytochrome C release from the mitochondria and activated caspase-9 cleavage (Green and Llambi, 2015;Liu et al, 2020;Yon et al, 2005). Phosphorylation of antiapoptotic MCL1 can be activated by stress and mitotic kinases such as AMP-activated protein kinase (MAPK), p38 MAPK, casein kinase II, Jun amino-terminal kinase (JNK) (Wertz et al, 2011), and growth factor and phosphoinositide 3-kinase (PI3K)-AKT-glycogen synthase kinase (GSK) 3 signaling (Maurer et al, 2006).…”
Section: Neural Cell Deathmentioning
confidence: 99%