Effects of subanesthetic ketamine on regional cerebral glucose metabolism in humans
Effects of subanesthetic ketamine on regional cerebral glucose metabolism in humans
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DOI：
10.1097/00000542-200405000-00006
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发表时间：
2004-05-01
期刊：
影响因子：
8.8
通讯作者：
Scheinin, H
中科院分区：
文献类型：
--
作者：
Långsjö, JW;Salmi, E;Scheinin, H
背景：作者最近用正电子发射断层扫描显示，亚麻醉剂量的外消旋氯胺酮增加脑血流量，但不显著影响氧消耗。在这项研究中，作者希望评估在类似条件下外消旋氯胺酮对区域葡萄糖代谢率（rGMR）的影响，以确定氯胺酮是否真的引起脑血流和代谢之间的紊乱耦合。方法：使用f -18标记的氟脱氧葡萄糖作为正电子发射断层扫描示踪剂，量化9名健康男性志愿者在基线和300-ng/ml氯胺酮目标浓度水平下12个感兴趣脑区的rGMR。此外，利用统计参数映射对rGMR的相对变化进行了基于体素的分析。结果：+/- SD测定氯胺酮血清浓度平均值为326.4 +/- 86.3 ng/ml。氯胺酮输注期间平均动脉压略有升高（最大升高16.4%）（P < 0.001）。在大多数感兴趣的研究区域，氯胺酮显著增加绝对rGMR。其中，丘脑（14.6 +/- 15.9%,P = 0.029）、额叶（13.6 +/- 13.1%,P = 0.011）和顶叶皮质（13.1 +/- 11.2%,P = 0.007）增加最多。绝对rGMR在大脑的任何地方都没有下降。基于体素的分析显示，额叶、颞叶和顶叶皮层的rGMR相对增加。结论：rGMR的全球增加似乎与作者早期研究中发现的氯胺酮引起的脑血流量增加相似。因此，氯胺酮引起的脑血流量和代谢之间耦合的干扰是极不可能的。先前观察到的氧提取部分的减少可能是由于氯胺酮诱导谷氨酸释放增加时的非氧化糖代谢。
Background: The authors have recently shown with positron emission tomography that subanesthetic doses of racemic ketamine increase cerebral blood How but do not affect oxygen consumption significantly. In this study, the authors wanted to assess the effects of racemic ketamine on regional glucose metabolic rate (rGMR) in similar conditions to establish whether ketamine truly induces disturbed coupling between cerebral blood flow and metabolism.Methods: F-18-labeled fluorodeoxyglucose was used as a positron emission tomography tracer to quantify rGMR on 12 brain regions of interest of nine healthy male volunteers at baseline and during a 300-ng/ml ketamine target concentration level. in addition, voxel-based analysis was performed for the relative changes in rGMR using statistical parametric mapping.Results: The mean +/- SD measured ketamine serum concentration was 326.4 +/- 86.3 ng/ml. The mean arterial pressure was slightly increased (maximally by 16.4%) during ketamine infusion (P < 0.001). Ketamine increased absolute rGMR significantly in most regions of interest studied. The greatest increases were detected in the thalamus (14.6 +/- 15.9%; P = 0.029) and in the frontal (13.6 +/- 13.1%; P = 0.011) and parietal cortices (13.1 +/- 11.2%; P = 0.007). Absolute rGMR was not decreased anywhere in the brain. The voxel-based analysis revealed relative rGMR increases in the frontal, temporal, and parietal cortices.Conclusions: Global increases in rGMR seem to parallel ketamine-induced increases in cerebral blood flow detected in the authors' earlier study. Therefore, ketamine-induced disturbance of coupling between cerebral blood flow and metabolism is highly unlikely. The previously observed decrease in oxygen extraction fraction may be due to nonoxidative glucose metabolism during ketamine-induced increase in glutamate release.