From the Department of Anesthesiology, Shanghai Cancer Center, Fudan University, Shanghai, China.
School of Life Science and Technology.
Anesth Analg. 2022 Nov 1;135(5):1106-1114. doi: 10.1213/ANE.0000000000005869. Epub 2022 Jan 10.
Ketamine anesthesia increased glucose metabolism in most brain regions compared to another intravenous anesthetic propofol. However, whether the changes in cerebral metabolic networks induced by ketamine share the same mechanism with propofol remains to be explored. The purpose of the present study was to identify specific features of metabolic network in rat brains during ketamine-induced subanesthesia state and anesthesia state compared to awake state.
We acquired fluorodeoxyglucose positron emission tomography (FDG-PET) images in 20 healthy adult Sprague-Dawley rats that were intravenously administrated saline and ketamine to achieve different conscious states: awake (normal saline), subanesthesia (30 mg kg -1 h -1 ), and anesthesia (160 mg kg -1 h -1 ). Based on the FDG-PET data, the alterations in cerebral glucose metabolism and metabolic topography were investigated by graph-theory analysis.
The baseline metabolism in rat brains was found significantly increased during ketamine-induced subanesthesia and anesthesia. The graph-theory analysis manifested a reduction in metabolism connectivity and network global/local efficiency across cortical regions and an increase across subcortical regions during ketamine-induced anesthesia (nonparametric permutation test: global efficiency between awake and anesthesia, cortex: P = .016, subcortex: P = .015; global efficiency between subanesthesia and anesthesia, subcortex: P = .012).
Ketamine broadly increased brain metabolism alongside decreased metabolic connectivity and network efficiency of cortex network. Modulation of these cortical metabolic networks may be a candidate mechanism underlying general anesthesia-induced loss of consciousness.
与另一种静脉麻醉药异丙酚相比，氯胺酮麻醉会增加大脑大部分区域的葡萄糖代谢。然而，氯胺酮诱导的大脑代谢网络的变化是否与异丙酚具有相同的机制仍有待探索。本研究的目的是确定与清醒状态相比，氯胺酮诱导的亚麻醉状态和麻醉状态下大鼠大脑代谢网络的特定特征。
我们对 20 只健康成年 Sprague-Dawley 大鼠进行了氟脱氧葡萄糖正电子发射断层扫描（FDG-PET）成像，这些大鼠静脉注射生理盐水和氯胺酮，以达到不同的意识状态：清醒（生理盐水）、亚麻醉（30mg/kg/h）和麻醉（160mg/kg/h）。基于 FDG-PET 数据，通过图论分析研究了大脑葡萄糖代谢和代谢拓扑的变化。
在氯胺酮诱导的亚麻醉和麻醉期间，大鼠大脑的基础代谢被发现显著增加。图论分析显示，在氯胺酮诱导的麻醉过程中，大脑皮质区域的代谢连接和网络全局/局部效率降低，而皮质下区域的代谢连接和网络全局/局部效率增加（非参数置换检验：清醒与麻醉之间的全局效率，皮质：P=0.016，皮质下：P=0.015；亚麻醉与麻醉之间的全局效率，皮质下：P=0.012）。
氯胺酮广泛增加了大脑代谢，同时降低了皮质网络的代谢连接和网络效率。这些皮质代谢网络的调节可能是全麻诱导意识丧失的候选机制。
