Isoflurane anesthesia induced persistent, progressive memory impairment, caused a loss of neural stem cells, and reduced neurogenesis in young, but not adult, rodents
Isoflurane anesthesia induced persistent, progressive memory impairment, caused a loss of neural stem cells, and reduced neurogenesis in young, but not adult, rodents
复制标题
异氟烷麻醉会引起持续性、进行性记忆障碍，导致神经干细胞损失，并减少幼年啮齿动物（但不是成年啮齿动物）的神经发生
DOI：
10.1038/jcbfm.2009.274
复制
发表时间：
2010-05-01
影响因子：
6.3
通讯作者：
Blomgren, Klas
中科院分区：
文献类型：
--
作者：
Zhu, Changlian;Gao, Jianfeng;Blomgren, Klas
异氟烷和相关麻醉剂广泛用于麻醉儿童，从早产儿到青少年。人们对这些麻醉剂在儿科患者中的安全性提出了担忧，特别是对认知可能产生的负面影响。本研究的目的是研究幼年和成年动物重复接触异氟烷对认知和神经发生的影响。出生后第14天（P14）的大鼠和小鼠以及成年（P60）大鼠每天用异氟烷麻醉35分钟，连续4天。评价了物体识别、位置学习和反转学习以及细胞死亡和细胞发生。对象识别和逆转学习显着受损，异氟烷治疗的年轻大鼠和小鼠，而成年动物不受影响，这些赤字变得更加明显，随着动物年龄的增长。海马干细胞池减少和持续减少的神经发生，随后导致异氟烷处理大鼠齿状回颗粒细胞神经元数量减少，从而导致记忆缺陷。海马中的祖细胞或神经元的细胞死亡没有增加的迹象。这些发现显示了一种以前未知的神经毒性机制，以明显的年龄依赖性方式导致认知缺陷。Journal of Cerebral Blood Flow & Metabolism（2010）30，1017-1030; doi：10.1038/jcbfm.2009.274; 2010年1月13日在线发表
Isoflurane and related anesthetics are widely used to anesthetize children, ranging from premature babies to adolescents. Concerns have been raised about the safety of these anesthetics in pediatric patients, particularly regarding possible negative effects on cognition. The purpose of this study was to investigate the effects of repeated isoflurane exposure of juvenile and mature animals on cognition and neurogenesis. Postnatal day 14 (P14) rats and mice, as well as adult (P60) rats, were anesthetized with isoflurane for 35 mins daily for four successive days. Object recognition, place learning and reversal learning as well as cell death and cytogenesis were evaluated. Object recognition and reversal learning were significantly impaired in isoflurane-treated young rats and mice, whereas adult animals were unaffected, and these deficits became more pronounced as the animals grew older. The memory deficit was paralleled by a decrease in the hippocampal stem cell pool and persistently reduced neurogenesis, subsequently causing a reduction in the number of dentate gyrus granule cell neurons in isoflurane-treated rats. There were no signs of increased cell death of progenitors or neurons in the hippocampus. These findings show a previously unknown mechanism of neurotoxicity, causing cognitive deficits in a clearly age-dependent manner. Journal of Cerebral Blood Flow & Metabolism (2010) 30, 1017-1030; doi: 10.1038/jcbfm.2009.274; published online 13 January 2010