Sakai T, Singh H, Mi W D, Kudo T, Matsuki A
Department of Anaesthesiology & Pain Management, University of Hirosaki School of Medicine, Japan.
Acta Anaesthesiol Scand. 1999 Feb;43(2):212-6. doi: 10.1034/j.1399-6576.1999.430216.x.
We studied the effect of variable doses of ketamine on the endpoints of hypnosis, e.g., unresponsiveness to verbal commands (UVC), loss of eyelash reflex (LER), and inhibition of body movement response with or without sneezing to nasal membrane stimulation (INBMR), and processed EEG variables, e.g., bispectral index (BIS), 95% spectral edge frequency (SEF) and median frequency (MF) during propofol infusion.
Forty-eight patients received either propofol infusion, 30 mg.kg-1.h-1 (Group P; n = 12) or ketamine bolus, 0.25, 0.5 or 0.75 mg i.v., followed by propofol infusion, 30 mg.kg-1.h-1 + variable dose ketamine infusion, 0.25, 0.5 or 0.75 mg.kg-1.h-1 (Groups PK0.25, PK0.5 and PK0.75; n = 12 each) until UVC, LER and INBMR. BIS, 95% SEF and MF values were monitored and recorded at the endpoints of hypnosis. Propofol and ketamine concentrations were measured at INBMR.
Propofol infusion, 30 mg.kg-1.h-1, induced UVC, LER and INBMR at BIS: 65 +/- 2, 63 +/- 9 and 33 +/- 7; 95% SEF: 17 +/- 3, 17 +/- 4 and 14 +/- 3; and MF values of 5 +/- 2, 5 +/- 3 and 3 +/- 2, respectively. With adjunctive ketamine (Groups PK0.5 and PK0.75), the hypnotic endpoints were achieved at higher BIS and 95% SEF values and lower propofol doses and concentrations as compared to Groups P and PK0.25 (9.9 +/- 5.8 and 9.4 +/- 3.4 vs. 13.4 +/- 4.5 and 14 +/- 5.8 micrograms.ml-1).
Our results suggest additive interaction between propofol and ketamine (Groups PK0.5 and PK0.75) for achieving the hypnotic endpoints; however, ketamine did not depress the EEG variables in proportion to its hypnotic effect. The paradoxically higher BIS and 95% SEF values at the hypnotic endpoints may be due to lower propofol concentrations and/or no effect of ketamine on the EEG variables.
我们研究了不同剂量氯胺酮对催眠终点的影响，例如对言语指令无反应（UVC）、睫毛反射消失（LER）以及对鼻黏膜刺激有无喷嚏反应的身体运动反应抑制（INBMR），并在丙泊酚输注期间处理了脑电图变量，例如脑电双频指数（BIS）、95%频谱边缘频率（SEF）和中位频率（MF）。
48例患者接受丙泊酚输注，30mg·kg-1·h-1（P组；n = 12）或静脉注射氯胺酮推注剂量0.25、0.5或0.75mg，随后丙泊酚输注，30mg·kg-1·h-1 + 氯胺酮可变剂量输注，0.25、0.5或0.75mg·kg-1·h-1（PK0.25组、PK0.5组和PK0.75组；每组n = 12），直至达到UVC、LER和INBMR。在催眠终点监测并记录BIS、95% SEF和MF值。在INBMR时测量丙泊酚和氯胺酮浓度。
丙泊酚输注30mg·kg-1·h-1时，在BIS值为65±2、63±9和33±7；95% SEF值为17±3、17±4和14±3；MF值为5±2、5±3和3±2时分别诱导出UVC、LER和INBMR。与P组和PK0.25组相比，联合使用氯胺酮（PK0.5组和PK0.75组）时，在更高的BIS和95% SEF值以及更低的丙泊酚剂量和浓度下达到催眠终点（9.9±5.8和9.4±3.4 vs. 13.4±4.5和14±5.8μg·ml-1）。
我们的结果表明丙泊酚和氯胺酮（PK0.5组和PK0.75组）之间存在相加作用以达到催眠终点；然而，氯胺酮对脑电图变量的抑制与其催眠效果不成比例。催眠终点时BIS和95% SEF值反常地更高可能是由于丙泊酚浓度较低和/或氯胺酮对脑电图变量无影响。
