Zhou Yuxi, Huang Shiqian, Zhang Tianhao, Deng Daling, Huang Li, Chen Xiangdong
Department of Anesthesiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; Institute of Anesthesia and Critical Care Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; Key Laboratory of Anesthesiology and Resuscitation (Huazhong University of Science and Technology), Ministry of Education, Wuhan, China.
Department of Anesthesiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; Institute of Anesthesia and Critical Care Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; Key Laboratory of Anesthesiology and Resuscitation (Huazhong University of Science and Technology), Ministry of Education, Wuhan, China.
Pharmacol Res. 2025 Feb;212:107593. doi: 10.1016/j.phrs.2025.107593. Epub 2025 Jan 7.
General anesthesia is administered to millions of individuals each year, however, the precise mechanism by which it induces unconsciousness remains unclear. While some theories suggest that anesthesia shares similarities with natural sleep, targeting sleep-promoting areas and inhibiting arousal nuclei, recent research indicates a more complex process. Emerging evidence highlights the critical role of corticothalamocortical circuits, which are involved in higher cognitive functions, in controlling arousal states and modulating transitions between different conscious states during anesthesia. The administration of general anesthetics disrupts connectivity within these circuits, resulting in a reversible state of unconsciousness. This review elucidates how anesthetics impair corticothalamocortical interactions, thereby affecting the flow of information across various cortical layers and disrupting higher-order cognitive functions while preserving basic sensory processing. Additionally, the role of the prefrontal cortex in regulating arousal through both top-down and bottom-up pathways was examined. These findings highlight the intricate interplay between the cortical and subcortical networks in maintaining and restoring consciousness under anesthesia, offering potential therapeutic targets for enhancing anesthesia management.
每年有数百万患者接受全身麻醉,然而,其诱导意识丧失的确切机制仍不清楚。虽然一些理论认为麻醉与自然睡眠有相似之处,作用于促进睡眠的区域并抑制觉醒核团,但最近的研究表明这一过程更为复杂。新出现的证据强调了参与高级认知功能的皮质-丘脑-皮质回路在控制麻醉期间的觉醒状态和调节不同意识状态之间转换方面的关键作用。全身麻醉药的使用会破坏这些回路内的连接性,导致可逆的意识丧失状态。本综述阐明了麻醉药如何损害皮质-丘脑-皮质相互作用,从而影响信息在各皮质层的流动,扰乱高级认知功能,同时保留基本感觉处理能力。此外,还研究了前额叶皮质通过自上而下和自下而上的途径调节觉醒的作用。这些发现突出了皮质和皮质下网络在麻醉状态下维持和恢复意识方面的复杂相互作用,为改善麻醉管理提供了潜在的治疗靶点。