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SmartTots and IARS News, Press Releases and EventsSmartTots – Perspectives from the Front Lines
Millions of children undergo surgery annually. Recent studies suggest there may be reason for concern. This video, featuring Dr. Dean Andropoulos, Dr. Peter Davis, and Dr. Caleb Ing, provides a summary as to why research is needed and the type that is needed.
SmartTots to Help Make Anesthetics and Sedatives Safer for Children
Dr. Janet Woodcock, director of the Center for Drug Evaluation and Research at the Food and Drug Administration, and Dr. Michael Roizen, of the International Anesthesia Research Society, unveil a new partnership that aims to make anesthesia safer for children.
Pediatric Anesthesia Questions and Myths-Mayo Clinic
Dr. Randall Flick at Mayo Clinic “debunks myths” and answers common questions raised by parents in regard to anesthesia.
Behavioural impairments after exposure of neonatal mice to propofol are accompanied by reductions in neuronal activity in cortical circuitry.
Both animal and retrospective human studies have linked extended and repeated general anaesthesia during early development with cognitive and behavioural deficits later in life. However, the neuronal circuit mechanisms underlying this anaesthesia-induced behavioural impairment are poorly understood.
Protective Effect of GM1 Attenuates Hippocampus and Cortex Apoptosis After Ketamine Exposure in Neonatal Rat via PI3K/AKT/GSK3β Pathway.
Ketamine is a widely used analgesic and anesthetic in obstetrics and pediatrics. Ketamine is known to promote neuronal death and cognitive dysfunction in the brains of humans and animals during development. Monosialotetrahexosyl ganglioside (GM1), a promoter of brain development, exerts neuroprotective effects in many neurological disease models. Here, we investigated the neuroprotective effect of GM1 and its potential underlying mechanism against ketamine-induced apoptosis of rats.
Singular and short-term anesthesia exposure in the developing brain induces persistent neuronal changes consistent with chronic neurodegenerative disease.
The potential adverse impact of inhalational anesthetics on the developing brain was highlighted by the addition of a medication warning by the U.S. Food and Drug Administration for their use in the pediatric population. To investigate mechanisms by which early life anesthesia exposure could induce long-term neuronal dysfunction, we exposed rats to 1 minimum alveolar concentration sevoflurane at 7 days of life.
Edaravone Alleviated Propofol-Induced Neurotoxicity in Developing Hippocampus by mBDNF/TrkB/PI3K Pathway.
Early-life exposure to general anesthetics may lead to neurotoxic consequences. While many animal models and some clinical studies have demonstrated the high sensitivity and vulnerability of the developing brain of the newborns to anesthetic neurotoxicity, the mechanism of this effect remains unclear.
Effect of dexmedetomidine on sevoflurane-induced neurodegeneration in neonatal rats.
Structural brain abnormalities in newborn animals after prolonged exposure to all routinely used general anaesthetics have raised substantial concerns for similar effects occurring in millions of children undergoing surgeries annually. Combining a general anaesthetic with non-injurious sedatives may provide a safer anaesthetic technique. We tested dexmedetomidine as a mitigating therapy in a sevoflurane dose-sparing approach.
Intranasal levosimendan prevents cognitive dysfunction and apoptotic response induced by repeated isoflurane exposure in newborn rats.
Anesthetic-induced toxicity in early life may lead to risk of cognitive decline at later ages. Notably, multiple exposures to isoflurane (ISO) cause acute apoptotic cell death in the developing brain and long-term cognitive dysfunction. This study is the first to investigate whether levosimendan (LVS), known for its protective myocardial properties, can prevent anesthesia-induced apoptotic response in brain cells and learning and memory impairment.