摘要
目的 观察氯胺酮或氯胺酮加咪唑安定麻醉下皮层兴奋性神经递质谷氨酸含量的变化 ,探讨氯胺酮对脑皮层谷氨酸的作用是否与意识状态有关。方法 采用脑内微透析技术检测大鼠脑皮层谷氨酸含量。用微量泵将氯胺酮分别以 60、80、10 0和 12 0mg·kg-1·h-1的速度持续静脉泵注(分别为K6 0 、K80 、K10 0 和K12 0 组 )。然后停止泵注氯胺酮 4 0分钟 ,调整氯胺酮泵速为 60mg·kg-1·h-1,咪唑安定 10mg/kg经腹腔注射 (K6 0 +M组 )。各组均同步收集微透析液以及监测左上肢正中神经体感诱发电位 (SEP)。结果 在K80 、K10 0 和K12 0 组 ,氯胺酮不同剂量与递质含量呈明显负相关 (r= - 0 85 6,P(r) <0 0 1)。SEP的N2 0 波潜伏期在K80 和K10 0 组间变化无统计学意义 ,在K12 0 组显著延长 (P <0 0 1) ;振幅随氯胺酮剂量增加而逐渐下降 ,并与剂量呈明显负相关 (P(r) <0 0 1)。在K6 0 、K80 和K6 0 +M组 ,虽然SEP潜伏期变化无统计学差异 ,但是脑皮层谷氨酸含量逐渐下降 (P <0 0 1) ,SEP的振幅也逐渐下降 (P <0 0 1)。结论 氯胺酮可使鼠脑皮层兴奋性神经递质谷氨酸含量呈剂量依赖性下降 ,腹腔注射苯二氮受体激动药咪唑安定可增强氯胺酮的镇痛作用 ,并引起皮层谷氨酸含量的显著下降 ,说明氯胺酮可作用于脑皮层内?
Objective To study the changes of glutamate (G) content in the contex during anesthesia of ketamine with or without midazolam to investigate the relationship between the effect of ketamine on glutamate concentration and consciousness.Methods Using the technic of microdialysis and high pressure liquid chromatography to dectect the glutamate content in the cortex of rats.Ketamine was infused intravenously at the rate of 60(group K 60 ),80(group K 80 ),100(group K 100 )or 120mg·kg -1 ·h -1 (group K 120 ).Midazolam 10mg/kg was injected simultaneously and ketamine infusing rate was changed to 60mg·kg -1 ·h -1 .Somatosensory evoked potential (SEP) was monitored and dialysate was collected.Results In the groups K 80 ,K 100 and K 120 ,the dose of ketamine infused was inversely correlated with the content of glutamate in a dose dependent manner ( r= -0 856, P (r) <0 01).There was no significant difference of SEP latency between the group of K 80 and K 100 .But a significant difference was observed at the rate of 120mg·kg -1 ·h -1 .Ketamine resulted in a dose dependent attenuation of SEP amplitudes accompanied by a significant decrease in glutamate concentration ( r= -0 743, P (r) <0 01).In the groups of K 60 ?K 80 and K 60 +M,glutamate concentration decreased significantly ( P< 0 01) and SEP amplitude depressed strongly ( P< 0 01), while the change of latency did not show any statistical significance.Conclusions From the in vivo microdialysis study in rats,excitatory glutamate energetic neurotransmission is inhibited by ketamine via NMDA receptor channel blockade in a dose dependent manner.Midazolam,a benzodiazepine GABA A receptor agonist, injection simultaneously shows the synergistic analgesic effects on ketamine with a significant decrease in the level of glutamate in the cerebral cortex,indicating that excitatory glutamate energetic neurotransmisson is inhibited and the activity of NMDA receptor is reduced by ketamine via NMDA receptor channel blockade.Afferent somatosensory is also reduced.But the attenuation of glutamate in the cerebral cortex and the synergistic analgesic effects with ketamine induced by midazolam is not in proportion to the changes of EEG.This seems to confirm that the inhibition of the cerebral cortex produced by ketamine is seperated from the state of consciousness.
出处
《临床麻醉学杂志》
CAS
CSCD
2001年第7期381-384,共4页
Journal of Clinical Anesthesiology
