异丙酚和七氟醚用于癫痫患者手术治疗的麻醉比较
摘要
目的比较异丙酚和七氟醚应用于癫痫患者手术治疗的麻醉,观察不同麻醉浓度麻醉药物对脑电图的影响及哪种药物对脑电图描记的影响更小,术后并发症更少,更适合此类病人的麻醉选择。
方法术前准备:术前一周停用抗癫痫药物,反复进行EEG对照描记并常规行CT及MRI检查寻找癫痫病因,明确致痫灶的位置。术前药:入室后肌注长托宁15ug/kg,不用其他术前药。记录病人麻醉诱导前的HR、SBP、DBP、SPO_2、BIS、SEF,收集术前的EEG资料。
麻醉方案:两组患者均选择气管内插管全麻,麻醉诱导T组:瑞芬太尼1～2ug/kg,咪唑安定0.05mg/kg,维库溴铵0.1mg/kg,接着用异丙酚2～2.5mg/kg静脉注射,缓慢诱导行气管内插管,机控通气,术中维库溴铵间断静脉注射以维持满意的肌松。S组:维库溴铵0.1mg/kg,七氟醚吸入诱导,瑞芬太尼1-2ug/kg,咪唑安定0.05mg/kg静脉注射,维库溴铵0.1mg/kg,于肺泡气七氟醚达到1.5MAC时行气管插管,余同A组。以TOF监测肌松,维持T4/T1＜25%。入手术室(T_1)、麻醉插管时(T_2)、切开硬脑膜时(T_3)、七氟醚吸入浓度1.5MAC或异丙酚靶控浓度稳定在4.5ug/ml(T_4)、七氟醚吸入浓度为1.0MAC或异丙酚靶控浓度稳定在3μg/ml(T_5)、七氟醚吸入浓度0.5MAC或异丙酚靶控浓度稳定在1.5μg/ml(T_6)、拔管时刻(T_7);SBP、DBP、HR、SEF、BIS、PeTCO_2、SpO_2上述各项指标,并监测尿量,记录各时间点七氟醚吸入及呼出浓度、异丙酚靶控输注浓度,在切开硬脑膜后分别调整麻醉药物浓度稳定10分钟,再进行皮层脑电图描记,记录各描记点麻醉药物的浓度,比较各麻醉药物浓度对脑电图的影响。记录病人从停药至病人清醒的时间、拔管时间、手术时间及麻醉时间。术后24小时内回访病人,是否出现恶心、呕吐、躁动等麻醉相关并发症。
结果1.两组病人术前基本情况比较差异无统计学意义(表1)。
2.两组患者SBP、DBP、HR、BIS、SEF的基础值(T_1)比较其差异无显著性(P＞0.05)。两组患者SBP、DBP、HR、BIS、SEF等指标,T_2、T_3、T_4、T_5与T_1比较各时间点组内比较均有所下降,差异有显著性(P＜0.05)。
3.异丙酚与七氟醚两组病人T_4、T_5、T_6三个时刻皮层脑电图比较,T_4时刻记录到的棘波,棘尖波受到抑制,但仍能记录到,与T_5、T_6比较α波减少,β波及δ波增加,EEG波幅减低,在T_5、T_6时刻均能较好的描记定位癫痫病灶,未发现对癫痫波的强烈抑制与激发,说明七氟醚吸入浓度在1MAC或异丙酚靶控浓度在3ug/ml以下均能不影响术中脑电图的定位,但此两类药物对脑电图影响呈剂量依赖。
4.两组病人T_4时刻与T_5、T_6时刻比较BIS、SEF差异有显著性(P＜0.05),随着麻醉药物浓度的降低而增大,相同时刻组间比较差异无显著性(P＞0.05),SBP、DBP、HR比较差异无显著性。
5.术后24小时随访,两组病人均无术中知晓,术后恶心、呕吐、躁动比例S组高于T组,差异有显著性(P＜0.05)。
结论七氟醚和异丙酚对癫痫病人术中脑电图的影响有剂量依赖性,七氟醚吸入浓度在1MAC以下,异丙酚靶控浓度在3ug/ml以下时均可准确描记到癫痫波,亦未发现诱发异常棘波。麻醉加深时均表现为α波减少,β波及δ波增加,癫痫波较浅麻醉时表现出抑制。两组病人均未出现脑电图描记失真的情况。两种药物均可安全用于此类病人的麻醉,在一定麻醉深度下均不会影响皮层脑电图对癫痫的描记,苏醒时间与拔管时间两组之间比较差异没有显著性,但异丙酚麻醉后并发症发生率明显低于七氟醚。
Objective To compare propofol and sevoflurane used in the treatment of patients with epilepsy surgery anesthesia,observation the impact to the EEG monitor of different concentration of narcotic drugs and which have the smaller impact on the EEG monitor,less postoperative complications,More suitable for such patients to use in anesthesia.
Methods Preoperative preparation:in the previous week suspend antiepileptic drugs,check EEG repeatedly and make CT and MRI examination conventionally to find the cause of epilepsy and get the position of epileptic foci.Preoperative Medicine: after patient enter into the operating room intramuscular injection Penehyclidine Hydrochloride of 15 ug/kg,before the induction of anesthesia,record patients'HR、SBP、DBP、SPO_2、BIS and the SEF,collected the EEG before the operating.Anesthesia options:we choose general anesthesia endotracheal intubation for both groups of patients,the anesthesia Induction of group T:Vecuronium bromide 0.1mg/kg,then TCI propofol,we set the start target concentration at 5～7g/ml, remifentanil 0.2～0.5ug/kg.min,midazolam 0.05mg/kg intravenous injection,induced by the slow trip tracheal intubation,machine controlled Ventilation,during the operation we intermittent intravenous injection vecuronium to maintain the satisfanction of muscle relaxants.Group S:Vecuronium 0.1mg/kg,sevoflurane inhalation induction,remifentanil 0.2～0.5ug/kg.min and midazolam 0.05mg/kg intravenous injection,when the sevoflurane in alveolar reach 1.5 MAC,then we tracheal intubation,the others are the same as group T.Before the induction of anesthesia(T_1),15 minutes after intubation(T_2),when incision the dura(T_3); 1.3MAC or 4.5μg/ml(T_4);1.0MAC or 3μg/ml(T_5);0.5 MAC or 1.5μg/ml(T_6); extubation(T_7);SEF、MF、BIS、PeTCO_2、SpO_2、MAP、HR、BP in indicators,and monitoring urine output,recorded sevoflurane inhalation and exhaled concentrations at different time points,target-controlled infusion of propofol,incision in the dura mater to narcotic drugs respectively concentration in the concentration we set by in the concentration stability after 10 minutes then do EEG monitor,EEG was analysised by the professionals Comparison of preoperative and intraoperative localization EEG with different coconcentration narcotic drugs and whether they are consistent with different concentrations of the impact of the EEG.
Results:
1.Basic conditions of the Two groups patients have no statistically significant difference(Table 1).
2.Two groups of patients with SBP、DBP、HR、BIS、SEF basic value(T_1)compared the difference was not statistically significant(P＞0.05).Two groups of patients with SBP、DBP、HR、BIS、SEF indicators such as T_2、T_3、T_4、T_5 all time points compared with T_1 in the same group were declined,there were significant differences(P＜0.05).
3.Propofol and sevoflurane,in the two groups of patients T_4、T_5、T_6 cortical EEG three time points,T_4 time recorded spikes、spike sharp waves were suppressed,it has been able to be recorded,compared with the T_5 and T_6αwave reductionβandδincreased,EEG amplitude reduction.In the T_5 and T_6 moment can better monitor positioning epilepsy lesions found no the strong epilepsy wave excitation or inhibition, the concentration of sevoflurane inhalation below 1MAC or propofol,the target concentration below 3μg/ml can not affect get the positioning of EEG,but the effects of two types of drugs on the EEG were dose-dependent.
4.Compared T_4 with T_5、T_6 moment two groups of patients'SBP、DBP、HR、BIS、SEF,there were significant differences in the same group(P＜0.05),with the reduction of the concentration of narcotic drugs increased,in the same moment have no significant difference between two groups(P＞0.05).
5.Follow-up after 24 hours,two groups of patients showed no intraoperative awareness,postoperative nausea,vomiting,and sputum,restlessness group S ratio higher than T group,there were significant differences(P＜0.05).
Conclusion:sevoflurane and propofol,used in patients with epilepsy the effect of a dose-dependent manner in the EEG,sevoflurane inhalation in a concentration 1 MAC or below target-controlled propofol,below the concentration of 3μg/ml,can be credited to the accurate depiction of epilepsy wave and found no abnormal spikes induced,anesthesia will enhance both performance-αdecreasedβ-affected,but after the anesthesia of propofol,the incidence of anesthesia complications was significantly lower than sevoflurane group.Both two groups of patients had no distortion EEG monitored in the operation.
方法术前准备:术前一周停用抗癫痫药物,反复进行EEG对照描记并常规行CT及MRI检查寻找癫痫病因,明确致痫灶的位置。术前药:入室后肌注长托宁15ug/kg,不用其他术前药。记录病人麻醉诱导前的HR、SBP、DBP、SPO_2、BIS、SEF,收集术前的EEG资料。
麻醉方案:两组患者均选择气管内插管全麻,麻醉诱导T组:瑞芬太尼1～2ug/kg,咪唑安定0.05mg/kg,维库溴铵0.1mg/kg,接着用异丙酚2～2.5mg/kg静脉注射,缓慢诱导行气管内插管,机控通气,术中维库溴铵间断静脉注射以维持满意的肌松。S组:维库溴铵0.1mg/kg,七氟醚吸入诱导,瑞芬太尼1-2ug/kg,咪唑安定0.05mg/kg静脉注射,维库溴铵0.1mg/kg,于肺泡气七氟醚达到1.5MAC时行气管插管,余同A组。以TOF监测肌松,维持T4/T1＜25%。入手术室(T_1)、麻醉插管时(T_2)、切开硬脑膜时(T_3)、七氟醚吸入浓度1.5MAC或异丙酚靶控浓度稳定在4.5ug/ml(T_4)、七氟醚吸入浓度为1.0MAC或异丙酚靶控浓度稳定在3μg/ml(T_5)、七氟醚吸入浓度0.5MAC或异丙酚靶控浓度稳定在1.5μg/ml(T_6)、拔管时刻(T_7);SBP、DBP、HR、SEF、BIS、PeTCO_2、SpO_2上述各项指标,并监测尿量,记录各时间点七氟醚吸入及呼出浓度、异丙酚靶控输注浓度,在切开硬脑膜后分别调整麻醉药物浓度稳定10分钟,再进行皮层脑电图描记,记录各描记点麻醉药物的浓度,比较各麻醉药物浓度对脑电图的影响。记录病人从停药至病人清醒的时间、拔管时间、手术时间及麻醉时间。术后24小时内回访病人,是否出现恶心、呕吐、躁动等麻醉相关并发症。
结果1.两组病人术前基本情况比较差异无统计学意义(表1)。
2.两组患者SBP、DBP、HR、BIS、SEF的基础值(T_1)比较其差异无显著性(P＞0.05)。两组患者SBP、DBP、HR、BIS、SEF等指标,T_2、T_3、T_4、T_5与T_1比较各时间点组内比较均有所下降,差异有显著性(P＜0.05)。
3.异丙酚与七氟醚两组病人T_4、T_5、T_6三个时刻皮层脑电图比较,T_4时刻记录到的棘波,棘尖波受到抑制,但仍能记录到,与T_5、T_6比较α波减少,β波及δ波增加,EEG波幅减低,在T_5、T_6时刻均能较好的描记定位癫痫病灶,未发现对癫痫波的强烈抑制与激发,说明七氟醚吸入浓度在1MAC或异丙酚靶控浓度在3ug/ml以下均能不影响术中脑电图的定位,但此两类药物对脑电图影响呈剂量依赖。
4.两组病人T_4时刻与T_5、T_6时刻比较BIS、SEF差异有显著性(P＜0.05),随着麻醉药物浓度的降低而增大,相同时刻组间比较差异无显著性(P＞0.05),SBP、DBP、HR比较差异无显著性。
5.术后24小时随访,两组病人均无术中知晓,术后恶心、呕吐、躁动比例S组高于T组,差异有显著性(P＜0.05)。
结论七氟醚和异丙酚对癫痫病人术中脑电图的影响有剂量依赖性,七氟醚吸入浓度在1MAC以下,异丙酚靶控浓度在3ug/ml以下时均可准确描记到癫痫波,亦未发现诱发异常棘波。麻醉加深时均表现为α波减少,β波及δ波增加,癫痫波较浅麻醉时表现出抑制。两组病人均未出现脑电图描记失真的情况。两种药物均可安全用于此类病人的麻醉,在一定麻醉深度下均不会影响皮层脑电图对癫痫的描记,苏醒时间与拔管时间两组之间比较差异没有显著性,但异丙酚麻醉后并发症发生率明显低于七氟醚。
Objective To compare propofol and sevoflurane used in the treatment of patients with epilepsy surgery anesthesia,observation the impact to the EEG monitor of different concentration of narcotic drugs and which have the smaller impact on the EEG monitor,less postoperative complications,More suitable for such patients to use in anesthesia.
Methods Preoperative preparation:in the previous week suspend antiepileptic drugs,check EEG repeatedly and make CT and MRI examination conventionally to find the cause of epilepsy and get the position of epileptic foci.Preoperative Medicine: after patient enter into the operating room intramuscular injection Penehyclidine Hydrochloride of 15 ug/kg,before the induction of anesthesia,record patients'HR、SBP、DBP、SPO_2、BIS and the SEF,collected the EEG before the operating.Anesthesia options:we choose general anesthesia endotracheal intubation for both groups of patients,the anesthesia Induction of group T:Vecuronium bromide 0.1mg/kg,then TCI propofol,we set the start target concentration at 5～7g/ml, remifentanil 0.2～0.5ug/kg.min,midazolam 0.05mg/kg intravenous injection,induced by the slow trip tracheal intubation,machine controlled Ventilation,during the operation we intermittent intravenous injection vecuronium to maintain the satisfanction of muscle relaxants.Group S:Vecuronium 0.1mg/kg,sevoflurane inhalation induction,remifentanil 0.2～0.5ug/kg.min and midazolam 0.05mg/kg intravenous injection,when the sevoflurane in alveolar reach 1.5 MAC,then we tracheal intubation,the others are the same as group T.Before the induction of anesthesia(T_1),15 minutes after intubation(T_2),when incision the dura(T_3); 1.3MAC or 4.5μg/ml(T_4);1.0MAC or 3μg/ml(T_5);0.5 MAC or 1.5μg/ml(T_6); extubation(T_7);SEF、MF、BIS、PeTCO_2、SpO_2、MAP、HR、BP in indicators,and monitoring urine output,recorded sevoflurane inhalation and exhaled concentrations at different time points,target-controlled infusion of propofol,incision in the dura mater to narcotic drugs respectively concentration in the concentration we set by in the concentration stability after 10 minutes then do EEG monitor,EEG was analysised by the professionals Comparison of preoperative and intraoperative localization EEG with different coconcentration narcotic drugs and whether they are consistent with different concentrations of the impact of the EEG.
Results:
1.Basic conditions of the Two groups patients have no statistically significant difference(Table 1).
2.Two groups of patients with SBP、DBP、HR、BIS、SEF basic value(T_1)compared the difference was not statistically significant(P＞0.05).Two groups of patients with SBP、DBP、HR、BIS、SEF indicators such as T_2、T_3、T_4、T_5 all time points compared with T_1 in the same group were declined,there were significant differences(P＜0.05).
3.Propofol and sevoflurane,in the two groups of patients T_4、T_5、T_6 cortical EEG three time points,T_4 time recorded spikes、spike sharp waves were suppressed,it has been able to be recorded,compared with the T_5 and T_6αwave reductionβandδincreased,EEG amplitude reduction.In the T_5 and T_6 moment can better monitor positioning epilepsy lesions found no the strong epilepsy wave excitation or inhibition, the concentration of sevoflurane inhalation below 1MAC or propofol,the target concentration below 3μg/ml can not affect get the positioning of EEG,but the effects of two types of drugs on the EEG were dose-dependent.
4.Compared T_4 with T_5、T_6 moment two groups of patients'SBP、DBP、HR、BIS、SEF,there were significant differences in the same group(P＜0.05),with the reduction of the concentration of narcotic drugs increased,in the same moment have no significant difference between two groups(P＞0.05).
5.Follow-up after 24 hours,two groups of patients showed no intraoperative awareness,postoperative nausea,vomiting,and sputum,restlessness group S ratio higher than T group,there were significant differences(P＜0.05).
Conclusion:sevoflurane and propofol,used in patients with epilepsy the effect of a dose-dependent manner in the EEG,sevoflurane inhalation in a concentration 1 MAC or below target-controlled propofol,below the concentration of 3μg/ml,can be credited to the accurate depiction of epilepsy wave and found no abnormal spikes induced,anesthesia will enhance both performance-αdecreasedβ-affected,but after the anesthesia of propofol,the incidence of anesthesia complications was significantly lower than sevoflurane group.Both two groups of patients had no distortion EEG monitored in the operation.
引文
[1]Glass PA,Shafer SL,Reves JG..Intravenous drag delivery systems.In:Miller RD,eds.Anesthesia.5th ed.Harcount,Asia:Churchill Livingstone,2001.377-411.
[2]Nieuwenhuyzen MC,Engbers FH,Vuyk J,etal.Target controlled infusion systems:role in anesthesia and anaglgesia.Clin Pharmacokinet,2000,38:181-190.
[3]Slee TA,Larn AM.,Winn HR,etal.The cerebral hemodynamic and metabolic response to alfentanil in humans[J].Anesthesiology,1991,75(Supp13A):A171.
[4]王明山,几种新型麻醉药对脑功能的影响[J]。国外医学麻醉与复苏分册1996,17(1):16.
[5]丁布为,彭章龙,赵永泉。高龄病人异丙酚分步TCI时效应室浓度及BIS的变化。中华麻醉学杂志,2002,2(212):711-714.
[6]Kearse LA,RosowC,Zaslavsky A,etal.Bispectral analysis of electroencephalogram predicts conscious processing of information durin propofol sedation and hypnosis Anesthesiology 1998,88:25-34.
[7]Malinga M,Peitfaux F,Lepage JY,et l.Dose-response relationship between target-controlled oncentration of propofol and bispectral index.Br[J]Anaesth,1998,80.
[8]Glass P,Bloom M,Kearse,G etal,Bispectral analysis measures sedation and memory effects of propofol,midazolam,isflurane,analfentanil in healthy volunteers,Anesthesiology,1997.86:86-847.
[9]Flashon R,Sebel PS,Sigl J.Bispectral analysis of the EEG for monitoring the hypnotic effect of propofol and propofol/alfentanil Anesthesiology 1995,83:A514.
[10]Dio M,Gajraj RJ,Mantzaridis Het al.Relation-ship between calculated blood concentration of propofol and electrophysiol-ogical variables during emergence from anesthesia:comparison of bispectral index,spectral edge frequency,median frequency and auditory evoked potential index.Br J Anaesth,1997,78:180-184.
[11]Gajraj RJ,Doi M,Mantzaridis H,etal.Analysis of the EEG bispectrum auditory evoked potentials and the EEGpower spectrum during repeated transitions from consciousness to unconsiousness.Br J Anaesth,1998,80:46-52.
[12]Kear L,Roscow C,Sebel PS,etal.The bispectral index correlates with sedation/hypnosis and recall:comparison using multiple agents.Amesthesiology,1995,83:A507.
[13]谭启富.主编.癫痫外科学[M].南京:南京大学出版社,1995.216-227.
[14] Engel J .update on surgical treatment of the epilepsies :summary of the second international pulm desert conference on the surgical treatment of the epilepsies.neurology,1993,43:1612～1617.
[15] Danks RA ,Rogers M ,Aglio LS ,etal. Patient tolerance of craniotomy performed with the patient under local anesthesia and monitored conscious sedation. Neurosurgery , 1998,42 :28～36.
[16] Duffau H .Capelle L, Sichez J, etal. Intra2operative directelectrical stimulations of the central nervous system: the Salpetriere experience with 60 patients. Acta Neurochir J Clin Anesthesia October 2003,Vol. 19, No.10 (Wien) ,1999,141:1157～1167.
[17] Gumprecht H , Ebel GK,Auer DP , etal. Neuronavigation and functional MRI for surgery in patients with lesion in eloquent brain areas.Minim Invasive Neurosurg ,2002,45 :151～153.
[18] Frink EJ Jr, Malan TP, Morgan SE etal , Renal concentrating function with prolonged sevoflurane or enflurane anesthesia in volunteers. Anesthesiology. 1994 May;80(5):1019～25.
[19] Ebert TJ, Robinson BJ, Uhrich TD, etal , Recovery from sevoflurane anesthesia: a comparison to isoflurane and propofol anesthesia Anesthesiology. 1998 Dec;89(6): 1524-31.
[20] Polley JW, Berkowitz RA,Mc Donald TB, Cohen M, Figueroa A, Penney DW Plast Reconstr Surg. 1994 May;93(6): 1258-63. Scheller M.S etal Br J Anaesth ,1990;65:388
[21] Scheller MS, Nakakimura K, Fleischer JE, Zornow MH.Cerebral effects of sevoflurane in the dog: comparison with isoflurane and enflurane.Br J Anaesth. 1990 Sep;65(3):388～92.
[22] Osawa M, Shingu K, Murakawa M, Adachi T, Kurata J, Seo N, Murayama T, Nakao S, Mori K.Effects of sevoflurane on central nervous system electrical activity in cats.Anesth Analg. 1994 Jul;79(1):52～7.
[23] Lu DP, Lu GP, Reed JF 3rd.Safety, efficacy, and acceptance of intramuscular sedation: assessment of 900 dental cases.Compendium. 1994 Nov;15(11):1348,1350,1352 passim; quiz 1362.
[24] Strebel S etal.Cerebral vasomotor responsiveness to carbon dioxide is preserved during propofol and midazolam anesthesia in humans. Anesth Analg. 1994 May;78(5):884～8.
[25] Alkire MT, Haier RJ, Barker SJ, Shah NK etal, Cerebral metabolism during propofol anesthesia in humans studied with positron emission tomography Anesthesiology. 1995 Feb;82(2):393～403
[26] Alkire MT, Haier etal . Positron emission tomography study of regional cerebral metabolism in humans during isoflurane anesthesi, Anesthesiology. 1997 Mar;86(3):549～557.
[27] Alkire MT, Haier RJ, Barker SJ.etal, Cerebral metabolism during propofol anesthesia in humans studied with positron emission tomography. Anesthesiology. 1995 Feb;82(2):393～403.
[28] Pinaud M.Effects of systemic morphine and epidural bupivacaine on postoperative oxygen consumption during rewarming.J ClinAnesth. 1988;1(2):81～6.
[29] Frink EJ , Malan TP, Morgan SE, etal . Quantification of the degradation products of sevoflurane in two CO_2 absorbants during low-flow anesthesia in surgical patients Anesthesiology. 1992 Dec;77(6): 1064-9.
[30] Milde LN, Milde JH etal. The effects of dextrose infusion and head position on neurologic outcome after complete cerebral ischemia in primates: examination of a model. Anesthesiology. 1987 Jan;66(1):39～48.
[31] Robert E, Ripart J, Lefrant JY, Fabbro-Peray P, Eledjam JJ etal , Effects of halothane and enflurane on ventricular conduction, refractoriness, and wavelength: a concentration-response study in isolated hearts Anesthesiology. 1999 Dec;91(6):1873～1881.
[32] Knudsen L, Johansen UT, Jensen S etal, The effects of midazolam on cerebral blood flow and oxygen consumption. Interaction with nitrous oxide in patients undergoing craniotomy for supratentorial cerebral tumours. Anaesthesia. 1990 Dec;45(12):1016～1019.
[33] 白勤,王保国．异丙酚对癫痫病人脑电图的影响[J]．临床麻醉学杂志,1998,14(2)：106．
[34] Seifert HA ,Blouin RT ,Conard PA etal. Sedative doses of propofol increase Beta activity of the processed electroencephalogram [J]. Anesth Analg, 1993 ,76:976.
[35] Evers A. etal Cellular and molecular mechanisms of anesthesia. In: Paul G,Bruce F, Robert K, eds. Clinical anesthesia. 4th ed. Bosten: Williams Wilkins, 2001.12
[36] Sakai T, singh H. Mi WD, etal, The effect ofketamine or clinical end points of hypnosis and EEG variables during propofol infusion , Acta anaesthesiol scand. 1999,43: 212-216
[37] Kalkman CJ , Boezeman EH , Ribberink AA , et all Influence of changes in arterial carbon dioxide tension on the electroencephalogram and posterior tibial nerve somatosensorycortical evoked potentials during alfentanil/ nitrous oxide anesthesial Anesthesiology,1991,75:682-741
[38]Kennealy JA,Penovich PE,Moore Nease SE1 EEG and spectral analysis in acute hyperventilationl Electroenceph Clin Neurophsiol,1986,63:982-1061
[39]Patel VM,Maulsby RL1 How hyperventilation alters the electroencephalogram:a review of controversial viewpoints emphasizing neurophysiological mechanismsl J Clin Neurophysiol,1987,4:1012-120l
[40]刘俊杰,赵俊主编.现代麻醉学.北京:人民卫生出版社,1987,1141.
[41]Appadu BL,Lambert BG et al,Anaestetic agents with 5-HT_3 receptors,Anesth Analg,1994,79:1191-1192.
[42]Barann M,Gothert M,Fink K,etal Inhibition by anesthetics of,14C-guanidinum NIE-115neuroblastoma cells Naunyn Schmiedebergs Arch Pharmacol,1993,347:1252-1321.
[43]Gan TJ,E12Molem H,Ray J etal.Patient2controlled antiemesis arandomized,double blind comparison of two doses of propofol versus placebo[J].Anesthesiology,1999,90(6):1564-1570.
[44]Nakano M,FujiY et al.Prevention of nausea and vomiting after dental surgery:acomparison of small doses of propofol,droperidol,and metoclopramide.Can[J]Anaesth 2003,50:1085.
[45]Guignard B,Bossard AE,coste C,et al Acute opioid tolerance:intra operative remifentanil increases postoperative pain and morphine requirement,Anesthesiology 2000;93:409-417.
[46]Angst MS,Koppert W,pahl I,clark DJ,schmelzm M;short-term infusion of the mu-opiocd agonist remifentanil in humans causes hyperalgesia during with drawal,pain 2003;106:49-57.
[47]Simonnet G,Rivatc et al.opioid-induced hyperalgesia:Abnormal or normal pain,neuroreport 2003;14:1-7.
[1] Newton DEF. aneasthesia 1993; 48: 367
[2] 刘俊杰,赵俊主编．现代麻醉学．北京：人民卫生出版社,1987,1141．
[3] Pamp il IJ, Holzer JA, Quest DO, et al. Prognostic value of computerized EEG analysis during carotid endarterectomy. Anesth Analg, 1983,62:186.
[4] Shapiro HM , Drummond JC1 Neurosurgical anesthesia and intracranial hypertensionl In: Miller RD, edl Anesthesia, 3rd edn. New York: Churchill Livingstone, 1990.1737-1791.
[5] Smiley RM, Omstein E,Matteo RS, et al. Desflurane and isoflurane in surgical patientsxomparison of emergence time. Anesthesiology, 1991,74:425.
[6] Saidman LJ. The role of desflurane in the p ractice of anesthesia. Anesthesiology, 1991,74:399.
[7] Sebel PS ,Lang E ,Rampil IJ ,et al. A multicenter study of bispectral electroencephalogram analysis for monitoring anesthetic effect. Anesth Analg ,1997,84:891～889.
[8] Evers A.Cellular and molecular mechanisms of anesthesia.In: Paul G,Bruce F,Robert K, eds. Clinical anesthesia.Bosten: Williams Wilkins,2001.12.
[9] Sakai T, singh H, Mi WD, et al, The effect of ketamine or clinical end points of hypnosis and EEG variables during propofol infusion , Acta anaesthesiol scand, 1999, 43: 21-26
[10] Kalkman CJ , Boezeman EH , Ribberink AA, et all Influence of changes in arterial carbon dioxide tension on the electroencephalogram and posterior tibial nerve somatosensorycortical evoked potentials during alfentanil/ nitrous oxide anesthesial Anesthesiology, 1991,75 :68～74
[11] Kennealy JA , Penovich PE , Moore Nease SE1 EEG and spectral analysis in acute hyperventilationl Electroenceph Clin Neurophsiol ,1986 ,63:98～106.
[12] Kennealy JA, McLennan J E , Loudon RG, et all Hyperventilation induced cerebral hypoxial Am Rev Respir Dis, 1980,122 :407～412.
[13] Kraier V , van Huffelen AC , Wieneke GH1 Changes in quantitative EEG and blood flow velocity due to standardized hyperventilation:amodel of transient ischemia in young human subjectsl Electroenceph Clin Neurophsiol, 1988 ,70 :3772～3871.
[14] Patel VM , Maulsby RL1 How hyperventilation alters the electroencephalogram: a review of controversial viewpoints emphasizing neurophysiological mechanisms 1 J Clin Neurophysiol, 1987,4:1012-1201.
[15] Mathew JD.weather Wax KJ,East CJ,et al.Bispectral analysis during Cardiopulmonnay bypass:the effect of hypothermia on the hypnotic state,[J]Anesth,2001,13:301-305.
[16]Bruder N,Bonnet M,Epileptogenic drugs in anesthesiaJol Res,1999,21(6):535-540.
[2]Nieuwenhuyzen MC,Engbers FH,Vuyk J,etal.Target controlled infusion systems:role in anesthesia and anaglgesia.Clin Pharmacokinet,2000,38:181-190.
[3]Slee TA,Larn AM.,Winn HR,etal.The cerebral hemodynamic and metabolic response to alfentanil in humans[J].Anesthesiology,1991,75(Supp13A):A171.
[4]王明山,几种新型麻醉药对脑功能的影响[J]。国外医学麻醉与复苏分册1996,17(1):16.
[5]丁布为,彭章龙,赵永泉。高龄病人异丙酚分步TCI时效应室浓度及BIS的变化。中华麻醉学杂志,2002,2(212):711-714.
[6]Kearse LA,RosowC,Zaslavsky A,etal.Bispectral analysis of electroencephalogram predicts conscious processing of information durin propofol sedation and hypnosis Anesthesiology 1998,88:25-34.
[7]Malinga M,Peitfaux F,Lepage JY,et l.Dose-response relationship between target-controlled oncentration of propofol and bispectral index.Br[J]Anaesth,1998,80.
[8]Glass P,Bloom M,Kearse,G etal,Bispectral analysis measures sedation and memory effects of propofol,midazolam,isflurane,analfentanil in healthy volunteers,Anesthesiology,1997.86:86-847.
[9]Flashon R,Sebel PS,Sigl J.Bispectral analysis of the EEG for monitoring the hypnotic effect of propofol and propofol/alfentanil Anesthesiology 1995,83:A514.
[10]Dio M,Gajraj RJ,Mantzaridis Het al.Relation-ship between calculated blood concentration of propofol and electrophysiol-ogical variables during emergence from anesthesia:comparison of bispectral index,spectral edge frequency,median frequency and auditory evoked potential index.Br J Anaesth,1997,78:180-184.
[11]Gajraj RJ,Doi M,Mantzaridis H,etal.Analysis of the EEG bispectrum auditory evoked potentials and the EEGpower spectrum during repeated transitions from consciousness to unconsiousness.Br J Anaesth,1998,80:46-52.
[12]Kear L,Roscow C,Sebel PS,etal.The bispectral index correlates with sedation/hypnosis and recall:comparison using multiple agents.Amesthesiology,1995,83:A507.
[13]谭启富.主编.癫痫外科学[M].南京:南京大学出版社,1995.216-227.
[14] Engel J .update on surgical treatment of the epilepsies :summary of the second international pulm desert conference on the surgical treatment of the epilepsies.neurology,1993,43:1612～1617.
[15] Danks RA ,Rogers M ,Aglio LS ,etal. Patient tolerance of craniotomy performed with the patient under local anesthesia and monitored conscious sedation. Neurosurgery , 1998,42 :28～36.
[16] Duffau H .Capelle L, Sichez J, etal. Intra2operative directelectrical stimulations of the central nervous system: the Salpetriere experience with 60 patients. Acta Neurochir J Clin Anesthesia October 2003,Vol. 19, No.10 (Wien) ,1999,141:1157～1167.
[17] Gumprecht H , Ebel GK,Auer DP , etal. Neuronavigation and functional MRI for surgery in patients with lesion in eloquent brain areas.Minim Invasive Neurosurg ,2002,45 :151～153.
[18] Frink EJ Jr, Malan TP, Morgan SE etal , Renal concentrating function with prolonged sevoflurane or enflurane anesthesia in volunteers. Anesthesiology. 1994 May;80(5):1019～25.
[19] Ebert TJ, Robinson BJ, Uhrich TD, etal , Recovery from sevoflurane anesthesia: a comparison to isoflurane and propofol anesthesia Anesthesiology. 1998 Dec;89(6): 1524-31.
[20] Polley JW, Berkowitz RA,Mc Donald TB, Cohen M, Figueroa A, Penney DW Plast Reconstr Surg. 1994 May;93(6): 1258-63. Scheller M.S etal Br J Anaesth ,1990;65:388
[21] Scheller MS, Nakakimura K, Fleischer JE, Zornow MH.Cerebral effects of sevoflurane in the dog: comparison with isoflurane and enflurane.Br J Anaesth. 1990 Sep;65(3):388～92.
[22] Osawa M, Shingu K, Murakawa M, Adachi T, Kurata J, Seo N, Murayama T, Nakao S, Mori K.Effects of sevoflurane on central nervous system electrical activity in cats.Anesth Analg. 1994 Jul;79(1):52～7.
[23] Lu DP, Lu GP, Reed JF 3rd.Safety, efficacy, and acceptance of intramuscular sedation: assessment of 900 dental cases.Compendium. 1994 Nov;15(11):1348,1350,1352 passim; quiz 1362.
[24] Strebel S etal.Cerebral vasomotor responsiveness to carbon dioxide is preserved during propofol and midazolam anesthesia in humans. Anesth Analg. 1994 May;78(5):884～8.
[25] Alkire MT, Haier RJ, Barker SJ, Shah NK etal, Cerebral metabolism during propofol anesthesia in humans studied with positron emission tomography Anesthesiology. 1995 Feb;82(2):393～403
[26] Alkire MT, Haier etal . Positron emission tomography study of regional cerebral metabolism in humans during isoflurane anesthesi, Anesthesiology. 1997 Mar;86(3):549～557.
[27] Alkire MT, Haier RJ, Barker SJ.etal, Cerebral metabolism during propofol anesthesia in humans studied with positron emission tomography. Anesthesiology. 1995 Feb;82(2):393～403.
[28] Pinaud M.Effects of systemic morphine and epidural bupivacaine on postoperative oxygen consumption during rewarming.J ClinAnesth. 1988;1(2):81～6.
[29] Frink EJ , Malan TP, Morgan SE, etal . Quantification of the degradation products of sevoflurane in two CO_2 absorbants during low-flow anesthesia in surgical patients Anesthesiology. 1992 Dec;77(6): 1064-9.
[30] Milde LN, Milde JH etal. The effects of dextrose infusion and head position on neurologic outcome after complete cerebral ischemia in primates: examination of a model. Anesthesiology. 1987 Jan;66(1):39～48.
[31] Robert E, Ripart J, Lefrant JY, Fabbro-Peray P, Eledjam JJ etal , Effects of halothane and enflurane on ventricular conduction, refractoriness, and wavelength: a concentration-response study in isolated hearts Anesthesiology. 1999 Dec;91(6):1873～1881.
[32] Knudsen L, Johansen UT, Jensen S etal, The effects of midazolam on cerebral blood flow and oxygen consumption. Interaction with nitrous oxide in patients undergoing craniotomy for supratentorial cerebral tumours. Anaesthesia. 1990 Dec;45(12):1016～1019.
[33] 白勤,王保国．异丙酚对癫痫病人脑电图的影响[J]．临床麻醉学杂志,1998,14(2)：106．
[34] Seifert HA ,Blouin RT ,Conard PA etal. Sedative doses of propofol increase Beta activity of the processed electroencephalogram [J]. Anesth Analg, 1993 ,76:976.
[35] Evers A. etal Cellular and molecular mechanisms of anesthesia. In: Paul G,Bruce F, Robert K, eds. Clinical anesthesia. 4th ed. Bosten: Williams Wilkins, 2001.12
[36] Sakai T, singh H. Mi WD, etal, The effect ofketamine or clinical end points of hypnosis and EEG variables during propofol infusion , Acta anaesthesiol scand. 1999,43: 212-216
[37] Kalkman CJ , Boezeman EH , Ribberink AA , et all Influence of changes in arterial carbon dioxide tension on the electroencephalogram and posterior tibial nerve somatosensorycortical evoked potentials during alfentanil/ nitrous oxide anesthesial Anesthesiology,1991,75:682-741
[38]Kennealy JA,Penovich PE,Moore Nease SE1 EEG and spectral analysis in acute hyperventilationl Electroenceph Clin Neurophsiol,1986,63:982-1061
[39]Patel VM,Maulsby RL1 How hyperventilation alters the electroencephalogram:a review of controversial viewpoints emphasizing neurophysiological mechanismsl J Clin Neurophysiol,1987,4:1012-120l
[40]刘俊杰,赵俊主编.现代麻醉学.北京:人民卫生出版社,1987,1141.
[41]Appadu BL,Lambert BG et al,Anaestetic agents with 5-HT_3 receptors,Anesth Analg,1994,79:1191-1192.
[42]Barann M,Gothert M,Fink K,etal Inhibition by anesthetics of,14C-guanidinum NIE-115neuroblastoma cells Naunyn Schmiedebergs Arch Pharmacol,1993,347:1252-1321.
[43]Gan TJ,E12Molem H,Ray J etal.Patient2controlled antiemesis arandomized,double blind comparison of two doses of propofol versus placebo[J].Anesthesiology,1999,90(6):1564-1570.
[44]Nakano M,FujiY et al.Prevention of nausea and vomiting after dental surgery:acomparison of small doses of propofol,droperidol,and metoclopramide.Can[J]Anaesth 2003,50:1085.
[45]Guignard B,Bossard AE,coste C,et al Acute opioid tolerance:intra operative remifentanil increases postoperative pain and morphine requirement,Anesthesiology 2000;93:409-417.
[46]Angst MS,Koppert W,pahl I,clark DJ,schmelzm M;short-term infusion of the mu-opiocd agonist remifentanil in humans causes hyperalgesia during with drawal,pain 2003;106:49-57.
[47]Simonnet G,Rivatc et al.opioid-induced hyperalgesia:Abnormal or normal pain,neuroreport 2003;14:1-7.
[1] Newton DEF. aneasthesia 1993; 48: 367
[2] 刘俊杰,赵俊主编．现代麻醉学．北京：人民卫生出版社,1987,1141．
[3] Pamp il IJ, Holzer JA, Quest DO, et al. Prognostic value of computerized EEG analysis during carotid endarterectomy. Anesth Analg, 1983,62:186.
[4] Shapiro HM , Drummond JC1 Neurosurgical anesthesia and intracranial hypertensionl In: Miller RD, edl Anesthesia, 3rd edn. New York: Churchill Livingstone, 1990.1737-1791.
[5] Smiley RM, Omstein E,Matteo RS, et al. Desflurane and isoflurane in surgical patientsxomparison of emergence time. Anesthesiology, 1991,74:425.
[6] Saidman LJ. The role of desflurane in the p ractice of anesthesia. Anesthesiology, 1991,74:399.
[7] Sebel PS ,Lang E ,Rampil IJ ,et al. A multicenter study of bispectral electroencephalogram analysis for monitoring anesthetic effect. Anesth Analg ,1997,84:891～889.
[8] Evers A.Cellular and molecular mechanisms of anesthesia.In: Paul G,Bruce F,Robert K, eds. Clinical anesthesia.Bosten: Williams Wilkins,2001.12.
[9] Sakai T, singh H, Mi WD, et al, The effect of ketamine or clinical end points of hypnosis and EEG variables during propofol infusion , Acta anaesthesiol scand, 1999, 43: 21-26
[10] Kalkman CJ , Boezeman EH , Ribberink AA, et all Influence of changes in arterial carbon dioxide tension on the electroencephalogram and posterior tibial nerve somatosensorycortical evoked potentials during alfentanil/ nitrous oxide anesthesial Anesthesiology, 1991,75 :68～74
[11] Kennealy JA , Penovich PE , Moore Nease SE1 EEG and spectral analysis in acute hyperventilationl Electroenceph Clin Neurophsiol ,1986 ,63:98～106.
[12] Kennealy JA, McLennan J E , Loudon RG, et all Hyperventilation induced cerebral hypoxial Am Rev Respir Dis, 1980,122 :407～412.
[13] Kraier V , van Huffelen AC , Wieneke GH1 Changes in quantitative EEG and blood flow velocity due to standardized hyperventilation:amodel of transient ischemia in young human subjectsl Electroenceph Clin Neurophsiol, 1988 ,70 :3772～3871.
[14] Patel VM , Maulsby RL1 How hyperventilation alters the electroencephalogram: a review of controversial viewpoints emphasizing neurophysiological mechanisms 1 J Clin Neurophysiol, 1987,4:1012-1201.
[15] Mathew JD.weather Wax KJ,East CJ,et al.Bispectral analysis during Cardiopulmonnay bypass:the effect of hypothermia on the hypnotic state,[J]Anesth,2001,13:301-305.
[16]Bruder N,Bonnet M,Epileptogenic drugs in anesthesiaJol Res,1999,21(6):535-540.