Yu Deshui, Li Linji, Yuan Weiguo
Department of Anesthesiology, The Second People's Hospital of Yibin, Yibin 644000, Sichuan, PR China.
Department of Anesthesiology, Nanchong Central Hospital, The Second Clinical College of North Sichuan Medical College, Nanchong 637000, Sichuan, PR China.
Biomed Pharmacother. 2017 Mar;87:196-199. doi: 10.1016/j.biopha.2016.12.062. Epub 2017 Jan 2.
Mounting animal studies have demonstrated that almost all the clinically used general anesthetics could induce widespread neuroapoptosis in the immature brain. Alarmingly, some published findings have reported long-term neurocognitive deficits in response to early anesthesia exposure which deeply stresses the potential seriousness of developmental anesthetic neurotoxicity. However, the connection between anesthesia induced neuroapoptosis and subsequent neurocognitive deficits remains controversial. It should be noted that developmental anesthesia related neurotoxicity is not limited to neuroapoptosis. Early anesthesia exposure caused transient suppression of neurogenesis, ultrastructural abnormalities in synapse and alteration in the development of neuronal networks also could contribute to the long-term neurocognitive dysfunction. Understanding the mechanisms of developmental anesthetic neurotoxicity, especially by which anesthesia impairs brain function months after exposure, may lead to development of rational preventive and therapeutic strategies. The focus of present review is on some of those potential mechanisms that have been proposed for anesthesia induced cognitive decline.
越来越多的动物研究表明，几乎所有临床使用的全身麻醉剂都可在未成熟大脑中诱导广泛的神经细胞凋亡。令人担忧的是，一些已发表的研究结果报告了早期麻醉暴露后出现的长期神经认知缺陷，这深刻凸显了发育性麻醉神经毒性的潜在严重性。然而，麻醉诱导的神经细胞凋亡与随后的神经认知缺陷之间的联系仍存在争议。应当指出的是，与发育性麻醉相关的神经毒性并不局限于神经细胞凋亡。早期麻醉暴露导致神经发生的短暂抑制、突触超微结构异常以及神经网络发育改变，这些也可能导致长期神经认知功能障碍。了解发育性麻醉神经毒性的机制，尤其是麻醉在暴露数月后如何损害脑功能，可能会促成合理的预防和治疗策略的制定。本综述的重点是一些已被提出的导致麻醉诱导认知功能下降的潜在机制。
