Lee Jin Hwan, Zhang James, Wei Ling, Yu Shan Ping
Department of Anesthesiology, Emory University School of Medicine, Atlanta, GA 30322, USA.
Department of Neurology, Emory University School of Medicine, Atlanta, GA 30322, USA.
Exp Neurol. 2015 Oct;272:50-60. doi: 10.1016/j.expneurol.2015.03.028. Epub 2015 Apr 8.
Each year, about six million children, including 1.5 million infants, in the United States undergo surgery with general anesthesia, often requiring repeated exposures. However, a crucial question remains of whether neonatal anesthetics are safe for the developing central nervous system (CNS). General anesthesia encompasses the administration of agents that induce analgesic, sedative, and muscle relaxant effects. Although the mechanisms of action of general anesthetics are still not completely understood, recent data have suggested that anesthetics primarily modulate two major neurotransmitter receptor groups, either by inhibiting N-methyl-D-aspartate (NMDA) receptors, or conversely by activating γ-aminobutyric acid (GABA) receptors. Both of these mechanisms result in the same effect of inhibiting excitatory activity of neurons. In developing brains, which are more sensitive to disruptions in activity-dependent plasticity, this transient inhibition may have longterm neurodevelopmental consequences. Accumulating reports from preclinical studies show that anesthetics in neonates cause cellular toxicity including apoptosis and neurodegeneration in the developing brain. Importantly, animal and clinical studies indicate that exposure to general anesthetics may affect CNS development, resulting in long-lasting cognitive and behavioral deficiencies, such as learning and memory deficits, as well as abnormalities in social memory and social activity. While the casual relationship between cellular toxicity and neurological impairments is still not clear, recent reports in animal experiments showed that anesthetics in neonates can affect neurogenesis, which could be a possible mechanism underlying the chronic effect of anesthetics. Understanding the cellular and molecular mechanisms of anesthetic effects will help to define the scope of the problem in humans and may lead to preventive and therapeutic strategies. Therefore, in this review, we summarize the current evidence on neonatal anesthetic effects in the developmental CNS and discuss how factors influencing these processes can be translated into new therapeutic strategies.
在美国,每年约有600万儿童,其中包括150万婴儿,接受全身麻醉手术,且常常需要多次麻醉。然而,新生儿麻醉剂对发育中的中枢神经系统(CNS)是否安全,仍是一个关键问题。全身麻醉包括使用能产生镇痛、镇静和肌肉松弛作用的药物。尽管全身麻醉剂的作用机制仍未完全明确,但最近的数据表明,麻醉剂主要通过抑制N-甲基-D-天冬氨酸(NMDA)受体,或者相反地通过激活γ-氨基丁酸(GABA)受体,来调节两个主要的神经递质受体组。这两种机制都会产生抑制神经元兴奋性活动的相同效果。在对活动依赖性可塑性破坏更为敏感的发育中的大脑中,这种短暂的抑制可能会产生长期的神经发育后果。临床前研究的报告不断积累,表明新生儿使用的麻醉剂会导致发育中的大脑出现细胞毒性,包括细胞凋亡和神经退行性变。重要的是,动物和临床研究表明,接触全身麻醉剂可能会影响中枢神经系统发育,导致长期的认知和行为缺陷,如学习和记忆障碍,以及社会记忆和社会活动异常。虽然细胞毒性与神经功能障碍之间的因果关系仍不明确,但最近动物实验的报告显示,新生儿使用的麻醉剂会影响神经发生,这可能是麻醉剂产生慢性影响的一种潜在机制。了解麻醉作用的细胞和分子机制,将有助于明确人类问题的范围,并可能带来预防和治疗策略。因此,在本综述中,我们总结了目前关于新生儿麻醉剂对发育中的中枢神经系统影响的证据,并讨论如何将影响这些过程的因素转化为新的治疗策略。