Långsjö Jaakko W, Kaisti Kaike K, Aalto Sargo, Hinkka Susanna, Aantaa Riku, Oikonen Vesa, Sipilä Hannu, Kurki Timo, Silvanto Martti, Scheinin Harry
Turku PET Centre, University of Turku, Finland.
Anesthesiology. 2003 Sep;99(3):614-23. doi: 10.1097/00000542-200309000-00016.
Animal experiments have demonstrated neuroprotection by ketamine. However, because of its propensity to increase cerebral blood flow, metabolism, and intracranial pressure, its use in neurosurgery or trauma patients has been questioned.
15O-labeled water, oxygen, and carbon monoxide were used as positron emission tomography tracers to determine quantitative regional cerebral blood flow (rCBF), metabolic rate of oxygen (rCMRO2), and blood volume (rCBV), respectively, on selected regions of interest of nine healthy male volunteers at baseline and during three escalating concentrations of ketamine (targeted to 30, 100, and 300 ng/ml). In addition, voxel-based analysis for relative changes in rCBF and rCMRO2 was performed using statistical parametric mapping.
The mean +/- SD measured ketamine serum concentrations were 37 +/- 8, 132 +/- 19, and 411 +/- 71 ng/ml. Mean arterial pressure was slightly elevated (maximally by 15.3%, P < 0.001) during ketamine infusion. Ketamine increased rCBF in a concentration-dependent manner. In the region-of-interest analysis, the greatest absolute changes were detected at the highest ketamine concentration level in the anterior cingulate (38.2% increase from baseline, P < 0.001), thalamus (28.5%, P < 0.001), putamen (26.8%, P < 0.001), and frontal cortex (25.4%, P < 0.001). Voxel-based analysis revealed marked relative rCBF increases in the anterior cingulate, frontal cortex, and insula. Although absolute rCMRO2 was not changed in the region-of-interest analysis, subtle relative increases in the frontal, parietal, and occipital cortices and decreases predominantly in the cerebellum were detected in the voxel-based analysis. rCBV increased only in the frontal cortex (4%, P = 0.022).
Subanesthetic doses of ketamine induced a global increase in rCBF but no changes in rCMRO2. Consequently, the regional oxygen extraction fraction was decreased. Disturbed coupling of cerebral blood flow and metabolism is, however, considered unlikely because ketamine has been previously shown to increase cerebral glucose metabolism. Only a minor increase in rCBV was detected. Interestingly, the most profound changes in rCBF were observed in structures related to pain processing.
动物实验已证明氯胺酮具有神经保护作用。然而，由于其有增加脑血流量、代谢及颅内压的倾向，其在神经外科手术或创伤患者中的应用受到质疑。
使用15O标记的水、氧气和一氧化碳作为正电子发射断层扫描示踪剂，分别在9名健康男性志愿者的选定感兴趣区域，于基线时及氯胺酮浓度逐步升高（目标浓度为30、100和300 ng/ml）期间，测定定量局部脑血流量（rCBF）、氧代谢率（rCMRO2）和血容量（rCBV）。此外，使用统计参数映射对rCBF和rCMRO2的相对变化进行基于体素的分析。
测得的氯胺酮血清平均浓度±标准差分别为37±8、132±19和411±71 ng/ml。氯胺酮输注期间平均动脉压略有升高（最大升高15.3%，P<0.001）。氯胺酮以浓度依赖性方式增加rCBF。在感兴趣区域分析中，在最高氯胺酮浓度水平时，在前扣带回（较基线增加38.2%，P<0.001）、丘脑（28.5%，P<0.001）、壳核（26.8%，P<0.001）和额叶皮质（25.4%，P<0.001）检测到最大的绝对变化。基于体素的分析显示前扣带回、额叶皮质和岛叶的rCBF有明显相对增加。尽管在感兴趣区域分析中绝对rCMRO2未改变，但在基于体素的分析中，在额叶、顶叶和枕叶皮质检测到细微的相对增加，而主要在小脑检测到相对减少。rCBV仅在额叶皮质增加（4%，P = 0.022）。
亚麻醉剂量的氯胺酮可引起rCBF整体增加，但rCMRO2无变化。因此，局部氧摄取分数降低。然而，由于先前已证明氯胺酮可增加脑葡萄糖代谢，因此认为脑血流量与代谢的耦合紊乱不太可能。仅检测到rCBV有轻微增加。有趣的是，在与疼痛处理相关的结构中观察到rCBF的最显著变化。
