Dexmedetomidine mitigates sevoflurane-induced cell cycle arrest in hippocampus

Liu, Bo; Yu, Peixia; Zhang, Fuzhen; Dong, Zhao

doi:10.1007/s00540-018-2545-1

Cited by 23 publications

(20 citation statements)

References 40 publications

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“…DEX reduces the neurotoxicity of sevoflurane through many pathways: inhibiting apoptosis and autophagy [59], increasing the expression of tyrosine kinase B (TrkB) and BDNF, promoting neurocyte proliferation, maintaining nervous system function [60], inhibiting neuronal mitochondrial dynamin-related protein (Drp1) [37], and dosedependently activating the bone morphogenetic protein (BMP)/Smad pathway to regulate self-renewal, differentiation, proliferation, migration, and apoptosis of the neuro-cyte [61]. The multiple signal pathways we mentioned above show that DEX has played a significant role in neuroprotection during infant development, laying the foundation for the safe adhibition of DEX in children and pregnant women and solving the problem of general anesthesia drug selection for children.…”

Section: Reduces Neurotoxicity Of Anesthetics and Regulatesmentioning

confidence: 99%

Organ-Protective Effects and the Underlying Mechanism of Dexmedetomidine

Bao

Tang

2020

Mediators of Inflammation

112

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Dexmedetomidine (DEX) is a highly selective α2 adrenergic receptor (α2AR) agonist currently used in clinical settings. Because DEX has dose-dependent advantages of sedation, analgesia, antianxiety, inhibition of sympathetic nervous system activity, cardiovascular stabilization, and significant reduction of postoperative delirium and agitation, but does not produce respiratory depression and agitation, it is widely used in clinical anesthesia and ICU departments. In recent years, much clinical study and basic research has confirmed that DEX has a protective effect on a variety of organs, including the nervous system, heart, lungs, kidneys, liver, and small intestine. It acts by reducing the inflammatory response in these organs, activating antiapoptotic signaling pathways which protect cells from damage. Therefore, based on wide clinical application and safety, DEX may become a promising clinical multiorgan protection drug in the future. In this article, we review the physiological effects related to organ protection in α2AR agonists along with the organ-protective effects and mechanisms of DEX to understand their combined application value.

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Section: Reduces Neurotoxicity Of Anesthetics and Regulatesmentioning

confidence: 99%

Organ-Protective Effects and the Underlying Mechanism of Dexmedetomidine

Bao

Tang

2020

Mediators of Inflammation

112

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“…Dexmedetomidine has sedative, analgesic, and sympatholytic properties. Several preclinical studies have suggested that dexmedetomidine provides neuroprotective effects against volatile and intravenous anesthetics in young animal brains 10,11 . Moreover, a few case reports in neonates and young children have described the feasibility of anesthesia with dexmedetomidine‐remifentanil in different clinical scenarios 12‐14 .…”

Section: Discussionmentioning

confidence: 99%

Use of dexmedetomidine and opioids as the primary anesthetic in infants and young children: A retrospective cohort study

Efune

Longanecker

Alex

et al. 2020

Pediatric Anesthesia

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Background: Anesthetic regimens using dexmedetomidine and short-acting opioids have been suggested as potential alternatives to sevoflurane-based anesthesia in children. The primary aim of this study is to compare demographics, intraoperative characteristics, and complications of general anesthetics in which dexmedetomidine and opioids were used without sevoflurane, or in combination with a low sevoflurane concentration, in children 36 months old and younger. The secondary aim is to evaluate intraoperative bispectral index (BIS) values when available in these patients. Methods: General anesthetics performed between January 1, 2017, and May 1, 2018, in children 2 years and younger who received dexmedetomidine and remifentanil, with or without sevoflurane, were identified. Additional anesthetics performed during this time in children 36 months and younger who received dexmedetomidine and opioids and had BIS monitoring were also identified. Charts were reviewed for demographic and intraoperative variables, including drug administration and hemodynamic data.

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“…Because of this dichotomy, it has become important to identify prospective neuroprotective agents and techniques that could counteract or prevent anesthetic-induced toxicity. These agents may come in the form of mitochondrial fission inhibitors (Xu et al 2016), ROS scavengers (Boscolo et al 2012), caspase activity modulators (Chaparro et al 2013;Inoue et al 2004), AKT/GSK3␤ signaling pathway inhibitors (Tao et al 2016), endoplasmic reticulum stress inhibitors such as salubrinal (Ge et al 2015), or new, neuroprotective anesthetic agents (Alam et al 2017;Bo et al 2018). With the major focus of anesthetic-induced neurotoxicity on the mitochondria, researchers have been looking at ways to mitigate fission activation by targeting Drp1-mitochondrial interaction (Xu et al 2016) and mitochondrial permeability transition pore activation (Chen et al 2015;Lamarche et al 2013).…”

Section: Neuroprotective Strategiesmentioning

confidence: 99%

Anesthetics: from modes of action to unconsciousness and neurotoxicity

Iqbal

Thompson

Riaz

et al. 2019

Journal of Neurophysiology

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Modern anesthetic compounds and advanced monitoring tools have revolutionized the field of medicine, allowing for complex surgical procedures to occur safely and effectively. Faster induction times and quicker recovery periods of current anesthetic agents have also helped reduce health care costs significantly. Moreover, extensive research has allowed for a better understanding of anesthetic modes of action, thus facilitating the development of more effective and safer compounds. Notwithstanding the realization that anesthetics are a prerequisite to all surgical procedures, evidence is emerging to support the notion that exposure of the developing brain to certain anesthetics may impact future brain development and function. Whereas the data in support of this postulate from human studies is equivocal, the vast majority of animal research strongly suggests that anesthetics are indeed cytotoxic at multiple brain structure and function levels. In this review, we first highlight various modes of anesthetic action and then debate the evidence of harm from both basic science and clinical studies perspectives. We present evidence from animal and human studies vis-à-vis the possible detrimental effects of anesthetic agents on both the young developing and the elderly aging brain while discussing potential ways to mitigate these effects. We hope that this review will, on the one hand, invoke debate vis-à-vis the evidence of anesthetic harm in young children and the elderly, and on the other hand, incentivize the search for better and less toxic anesthetic compounds.

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Dexmedetomidine mitigates sevoflurane-induced cell cycle arrest in hippocampus

Cited by 23 publications

References 40 publications

Organ-Protective Effects and the Underlying Mechanism of Dexmedetomidine

Organ-Protective Effects and the Underlying Mechanism of Dexmedetomidine

Use of dexmedetomidine and opioids as the primary anesthetic in infants and young children: A retrospective cohort study

Anesthetics: from modes of action to unconsciousness and neurotoxicity

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