四种常用静脉麻醉药对老年病人血液动力学影响的比较

目的 探讨脑电双频指数(BIS)为50时，硫喷妥钠、丙泊酚、咪唑安定、依托咪酯用于老年病人全麻诱导的剂量及其对血液动力学的影响。方法 65岁以上的老年病人48例，随机分为四组：硫喷妥钠组，丙泊酚组，咪唑安定组，依托咪酯组。四组均缓慢静注，并且用HXD-1型脑电监测仪测量每例病人的BIS。当BIS逐渐下降至50时停止静注，分别于注药前、注药后1、3、5、10min用Rheo Cardio Monitor连续非创伤性血液动力监测仪记录和计算出血液动力学有关参数。结果 BP下降以丙泊酚组为显著。丙泊酚组和硫喷妥钠组的PEP/LVEF比值明显增加，但丙泊酚组＞硫喷妥钠组。除依托咪酯组以外其他各组的每搏指数(SD、心脏指数(CI)、射血速率(EV)和每搏功(LVP)均有不同程度的降低，但以丙泊酚组为显著。依托咪酯组体循环血管阻力(SVR)无明显变化，硫喷妥钠组和咪唑安定组均有不同程度的升高，以咪唑安定组为显著，丙泊酚组明显下降。舒张末容量(EDV)咪唑安定组明显下降，其他各组无明显变化。结论 四种静脉麻醉药对老年病人血液动力学的影响由大到小依次为丙泊酚＞咪唑安定＞硫喷妥钠＞依托咪酯。BIS为50时，老年病人各静脉麻醉药的等效剂量为硫喷妥钠4mg／kg、丙泊酚1．2mg／kg、咪唑安定0．16mg／kg、依托咪酯0．34mg／kg。对于心功能较差和血容量不足的老年病人全麻诱导，依托咪酯是首选的静脉麻醉诱导药。     

麻醉诱导期间咪达唑仑、异丙酚、依托咪酯及硫喷妥钠对脑血流速率的影响

目的 观察不同麻醉药物在麻醉诱导期间对大脑中动脉血流速率的影响.方法 40例病人随机分为4组(每组10例),麻醉诱导药物分别为咪达唑仑0.15mg/kg、异丙酚2mg/kg、依托咪酯0.3mg/kg和硫喷妥钠5mg/kg.给药3min后行气管内插管.麻醉维持采用1%七氟醚-66%氧化亚氮和氧气吸入,同时机械通气维持PETCO2在35～40mmHg.采用经颅多普勒监测仪(TCD),分别于诱导前和诱导1、2、3、5、10、15min测定大脑中动脉血流速率(V-MCA),同时记录动脉血压、心率及PETCO2.结果 给药后1min,异丙酚、依托咪酯和硫喷妥钠可使V-MCA明显降低(P＜0.05),而咪达唑仑组无显著变化(P＞0.05).气管插管后,4组病人的Vm-MCA,其中仅咪达唑仑组与基础值相比有显著差异(P＜0.05),而其他3组与基础值相比无统计学差异(P＞0.05).结论 对于非神经外科手术病人,诱导剂量的异丙酚、依托咪酯和硫喷妥钠对V-MCA的有一定程度的影响,而咪达唑仑影响较小;在对气管插管引起的脑血流速率波动的抑制方面咪达唑仑则作用较弱.     

硫喷妥钠和依托咪酯对氧自由基影响的比较

目的:比较硫喷妥钠、依托咪酯丙二醇制剂、依托咪酯乳剂对氧自由基的影响。方法:54例拟行全麻患者随机分成四组,分别给予生理盐水10ml、硫喷妥钠6mg/kg、依托咪酯丙二醇制剂或依托咪酯乳剂0.3mg/kg。贵要静脉取血测定红细胞SOD,血浆GSH、MDA及机体总抗氧化能力(T-AO)。结果:对照组SOD总量(T-SOD)无明显变化,但MDA明显升高,GSH、T-AO显著降低;应用硫喷妥钠后T-SOD、GSH轻度降低,MDA明显降低,T-AO则显著升高;两种依托咪酯组T-AO均保持在基础值水平,显著高于对照组。结论:依托咪酯丙二醇制剂、依托咪酯乳剂与硫喷妥钠一样对机体的抗氧化能力具有较好的保护作用。     

不同诱导方法对颅内压影响的比较

颅内手术要求麻醉平稳 ,全身和脑血液动力学稳定 ,避免颅内压增高 ,而麻醉诱导引起的心血管反应会导致血压和颅内压升高。本文对不同诱导方法对颅内压的影响进行比较 ,以寻求较为理想的诱导方法。资料与方法选择 30例ASAI～II级颅内手术病人 ,随机分成硫喷妥钠组 (T组 )、依托咪酯组 (Y组 )和丙泊酚组 (P组 ) ,每组1 0例。术前 30min肌注苯巴比妥钠 0 1 g、阿托品 0 5mg。麻醉诱导先静注芬太尼 2 μg/kg、咪唑安定 0 1mg/kg后 ,T组硫喷妥钠 4～ 5mg/kg ,Y组依托咪酯 0 3mg/kg、P组丙泊酚 3mg/kg分别静注 ,继而静注维库溴铵 0 1mg/…     

罗库溴铵静脉注射部位疼痛的减轻方法观察

临床常用的静脉麻醉药，其中不少可引起病人注射部位疼痛，据统计50％-100％病人在接受某些亚剂量静脉麻醉药时常主诉不适或疼痛，因此，临床上已提出一些减轻或解除注射部位疼痛的方法，例如先静脉注射咪畦唑仑、芬太尼和利多卡因；或先静脉注射丙泊酚或硫喷妥钠，然后再注射罗库溴铵等方法，     

硫喷妥钠和依托咪酯合并罗库溴铵快速诱导的比较

罗库溴铵是一种快速的非去极化肌松药。本文旨在观察比较硫喷妥钠和依托咪酯在合并运用罗库溴铵快速诱导后的插管条件,哪个更优? 方法 60例ASAⅠ～Ⅱ级,在全麻下行择期手术的病人,随机分为硫喷妥钠组和依托咪酯组,每组30例。硫喷妥钠组,快速诱导给予硫喷妥钠5mg·kg~(-1)、阿芬太尼10mg·kg~(-1)、罗库溴铵0.6mg·kg~(-1);依托咪酯组,给予依托咪酯0.3mg·kg~(-1),其他用药同硫喷妥钠组。在静注完罗库溴铵60s以后,由同一位有经验的麻醉医师,但其不知病人的用药情况,从喉镜检查、声带的状况、以及插管反应3个方面进行评价插管的条件。     

四种静脉麻醉药物对大鼠皮层脑片缺氧缺糖损伤的作用

目的 探讨四种常用静脉麻醉药物对大鼠皮层脑片缺氧缺糖损伤的作用。方法 建立大鼠皮层脑片缺氧缺糖损伤模型,设立对照组、缺氧缺糖损伤组、药物加损伤组,利用2,3,5-三苯基氯化四氮唑(TTC)染色定量比色方法,评价氯胺酮、异丙酚、咪达唑仑和硫喷妥钠对脑片损伤的保护作用。结果 随着缺氧缺糖损伤时间的延长,皮层脑片TTC染色程度明显降低,TTC染色反映的组织损伤百分率与孵育上清液乳酸脱氢酶(LDN)释放比活性呈正相关(r=0.9609,P<0.01)。对于缺氧缺糖损伤所致脑片TTC染色降低,不同浓度氯胺酮均能完全抑制;与损伤组比较。大剂量硫喷妥钠和咪达唑仑(400μmol·L~(-1)和10μmol·L~(-1)A值明显升高(P<0.01或0.05);小剂量异丙酚(1μmol·L~(-1))对脑片TTC染色降低无作用,大剂量(100μmol·L~(-1))加重TTC染色降低(P<0.01)。结论 对于大鼠皮层脑片缺氧缺糖损伤,四种静脉麻醉药物作用效果各不相同:临床麻醉剂量的氯胺酮具有明显保护作用,咪达唑仑和硫喷妥钠在超过临床使用范围的大剂量时有部分保护作用;大剂量异丙酚会加重大鼠皮层脑片的缺氧缺糖损伤。     

异丙酚、依托咪酯和咪达唑仑对大鼠肾组织缝隙连接功能的影响

目的 评价异丙酚、依托咪酯以及咪达唑仑对大鼠肾组织缝隙连接(GJ)功能的影响.方法 离体实验大鼠肾小管上皮细胞NRK52E,以1.0×105/ml密度接种于6孔培养板(2 ml/孔),采用随机数字表法,将其分为4组(n=6):对照组(C组)、异丙酚组(P组)、依托咪酯组(E组)和咪达唑仑组(M组).C组采用含10％胎牛血清的DMEM-F12培养液培养,P组、E组和M组分别于培养液中加入异丙酚、依托咪酯和咪达唑仑,终浓度分别为15、8、4 μmol/L,孵育1h,采用细胞接种荧光示踪法测定GJ功能.在体实验健康SPF级雄性大鼠24只,2月龄,体重220 ～ 280 g,采用随机数字表法,将其分为4组(n=6):异丙酚组(P组)、依托咪酯组(E组)和咪达唑仑组(M组)分别腹腔注射异丙酚、依托咪酯和咪达唑仑100、6和5 mg/kg,对照组(C组)给予等容量生理盐水,连续3d.最后1次给药后30 min时取肾皮质,采用在体荧光示踪法测定GJ功能.结果 离体与在体实验:与C组比较,P组和E组GJ功能降低(P＜0.05),M组GJ功能差异无统计学意义(P＞0.05).结论 异丙酚和依托咪酯可明显抑制NRK52E细胞及大鼠肾组织GJ功能,而咪达唑仑对其无影响.     

不同麻醉诱导对患者眼内压影响的比较

目的 比较异丙酚、咪达唑仑或依托咪酯复合舒芬太尼麻醉诱导对患者眼内压(IOP)的影响.方法 拟在全麻下择期手术患者45例,年龄20-40岁,ASA分级Ⅰ或Ⅱ级,按照随机数字表法,将其随机分为3组(n=15):异丙酚组(P组)、咪达唑仑组(M组)和依托咪酯组(E组).麻醉诱导:P组、M组和E组分别静脉注射异丙酚2.0 mg/kg、咪达唑仑0.2 mg/kg及依托咪酯0.3 mg/kg后,依次静脉注射舒芬太尼0.2 μg/kg与顺阿曲库铵0.2 mg/kg,行气管插管术.于麻醉诱导前l min(T0)、气管插管前(T1)、气管插管后即刻(T2)、气管插管后1 min(T3)和2 min(T4)时测定IOP和MAP.结果 与P组比较,M组和E组低眼压发生率降低(P＜0.01);与E组比较,P组和M组高眼压发生率降低(P＜0.05).P组、M组和E组MAP与IOP的相关系数分别为0.831、0.889和0.806(p＜0.05),相关系数组间比较差异无统计学意义(P＞0.05).结论 咪达唑仑复合舒芬太尼麻醉诱导对IOP影响较小,MAP的波动程度是麻醉诱导引起IOP变化的主要因素.     

依托咪酯和硫喷妥钠用于全麻诱导的对比观察

依托咪酯和硫喷妥钠用于全麻诱导的对比观察薛荣亮＊李有才＊吴举民＊依托咪酯（又名乙咪酯）为强效、短时、安全的非巴比妥类静脉催眠药。作者将依托咪酯应用于麻醉诱导，并与硫喷妥钠进行比较，结果发现其麻醉效果稍优于硫喷妥钠，尤其对循环系统干扰小，现报告如下。资...     

Direct effect of anesthetic inducers on the electromyographic signals of the adductor pollicis

OBJECTIVES: To analyze the effect of thiopental, propofol, etomidate and midazolam on electromyographic study of the adductor pollicis before muscle relaxation. PATIENTS AND METHOD: Prospective study of 96 adults ASA I-II patients (gynecologic surgery) by electromyographic (Reflexograph Datex) recording of the adductor pollicis every 20 seconds with train-of-four (TOF) stimuli. After giving informed consent, the patients were randomized for type of induction agent. We studied changes in T1 (amplitude of the first response to TOF) and the TOF-ratio (T4/T1). The induction agent (thiopental 5 mg/kg), propofol 3 mg/kg, midazolam 0.2 mg/kg or etomidate 0.3 mg/kg) was given by slow 30 s injection 100 s after calibration of the Relaxograph. Changes in T1 and the TOF-ratio were recorded until 240 s. RESULTS: The groups were statistically homogeneous. In the thiopental group, T1 readings at 20, 40, 60 and 80 s (control times) were statistically different from the readings at 180, 220 and 240 s (after administering thiopental). T1 was significantly different at 120 and 200 s in the etomidate group. CONCLUSIONS: Thiopental and etomidate induce slight muscle relaxation at the expense of a reduction in T1 without changing the TOF-ratio, an effect that might be useful for rapid induction. Propofol and midazolam do not affect the electromyogram of the adductor pollicis. Thus, propofol is the anesthetic induction agent of choice for clinical studies on non-depolarizing muscle relaxants given that it changes neither T1 nor the TOF-ratio.     

Effect of midazolam pretreatment on the intravenous toxicity of lidocaine with and without epinephrine in rats

The effect of the benzodiazepine midazolam on the intravenous toxicity of lidocaine with and without epinephrine was studied in male Sprague-Dawley rats. Test rats with and control rats without midazolam premedication (2.5 mg/kg intraperitoneally, 10% of the median dose that caused loss of the righting reflex in a third group of rats) were given 2% lidocaine with and without 10 micrograms/ml epinephrine intravenously in doses sufficient to construct log-dose response curves for both convulsant and lethal responses. In control rats the median convulsant dose (CD50) of lidocaine was 15.2 mg/kg given alone and 10.9 mg/kg with epinephrine (a statistically significant difference); respective values for the median lethal dose (LD50) were 26.4 and 18.5 mg/kg (also statistically significant). While epinephrine enhanced lidocaine seizure activity and lethality by approximately 50%, midazolam almost completely prevented lidocaine-induced convulsions but had no significant effect on mortality.     

Inotropic Effects of Propofol, Thiopental, Midazolam, Etomidate, and Ketamine on Isolated Human Atrial Muscle

Background: Cardiovascular instability after intravenous induction of anesthesia may be explained partly by direct negative inotropic effects. The direct inotropic influence of etomidate, ketamine, midazolam, propofol, and thiopental on the contractility of isolated human atrial tissue was determined. Effective concentrations were compared with those reported clinically.

Methods: Atrial tissue was obtained from 16 patients undergoing coronary bypass surgery. Each fragment was divided into three strips, and one anesthetic was tested per strip in increasing concentrations (10 sup -6 to 10 sup -2 M). Strips were stimulated at 0.5 Hz, and maximum isometric force was measured. Induction agents were studied in two groups, group 1 (n = 7) containing thiopental, midazolam, and propofol, and group 2 (n = 9) consisting of etomidate, ketamine, and propofol.

Results: The tested anesthetics caused a concentration-dependent depression of contractility resulting in complete cessation of contractions at the highest concentrations. The IC50 S (mean +/-SEM; micro Meter) for inhibition of the contractility were: thiopental 43+/-7.6, propofol 235+/-48 (group 1), and 246+/-42 (group 2), midazolam 145+/-54, etomidate 133 +/-13, and ketamine 303+/-54.     

Comparison of etomidate, ketamine, midazolam, propofol, and thiopental on function and metabolism of isolated hearts.

The authors examined direct myocardial and coronary vascular responses to the anesthetic induction agents etomidate, ketamine, midazolam, propofol, and thiopental and compared their effects on attenuating autoregulation of coronary flow as assessed by changes in oxygen supply/demand relationships. Spontaneous heart rate, atrioventricular conduction time during atrial pacing, left ventricular pressure (LVP), coronary flow (CF), percent oxygen extraction, oxygen delivery, and myocardial oxygen consumption (MVo2) were examined in 55 isolated guinea pig hearts divided into five groups of 11 each. Hearts were perfused at constant pressure with one of the drugs administered at steady-state concentrations increasing from 0.5 microM to 1 mM. Adenosine was given to test maximal CF. At concentrations below 10 microM no significant changes were observed; beyond 50 microM for midazolam, etomidate, and propofol, and 100 microM for thiopental and ketamine, each agent caused progressive but differential decreases in heart rate, atrioventricular conduction time (leading to atrioventricular dissociation), LVP, +dLVP/dtmax, percent oxygen extraction, and MVo2. The concentrations (microM) at which +dLVP/dtmax was reduced by 50% were as follows: etomidate, 82 +/- 2 (mean +/- SEM); propofol, 91 +/- 4; midazolam, 105 +/- 8; thiopental, 156 +/- 11; and ketamine, 323 +/- 7; the rank order of potency was etomidate = propofol = midazolam greater than thiopental greater than ketamine; results were similar for LVP. At the 100 microM concentration, CF was decreased 11% +/- 2% by ketamine and 5% +/- 3% by thiopental but was increased 17% +/- 6% by etomidate, 21% +/- 5% by midazolam, and near maximally to 57% +/- 10% by propofol; MVo2 was decreased 8% +/- 4% by thiopental, 10% +/- 5% by ketamine, 19% +/- 5% by midazolam, 29% +/- 7% by etomidate, and 37% +/- 5% by propofol; oxygen delivery/MVo2 was unchanged by thiopental and ketamine but was increased 62% +/- 7% by midazolam, 71% +/- 9% by etomidate, and 150% +/- 15% by propofol. Between 100 microM and 1 mM, thiopental and ketamine did not increase CF but decreased MVo2 and percent oxygen extraction, whereas propofol maximally increased CF and decreased MVo2 and midazolam and etomidate had intermediate effects. These results indicate that on a molar basis, propofol, and less so midazolam and etomidate, depress cardiac function moderately more than thiopental and ketamine, and that propofol markedly attenuates autoregulation by causing coronary vasodilation. With doses used to induce anesthesia, propofol and thiopental appear to depress cardiac function more than ketamine or etomidate.     

Midazolam reduces the dose of propofol required for induction of anaesthesia and laryngeal mask airway insertion

BACKGROUND AND OBJECTIVE: Insertion of the laryngeal mask airway in the anaesthetized patient can sometimes be difficult and propofol has been advocated as the anaesthetic induction agent of choice because of its depressant effect on laryngeal reflexes compared with other intravenous anaesthetics. However, when used as the sole induction agent, relatively large doses of propofol are required to achieve successful laryngeal mask insertion. This has cost implications and may produce unwanted cardiorespiratory depression. METHODS: One hundred and forty-two patients were randomized to receive either: fentanyl 1 microg kg(-1) and lidocaine 1.5 mg kg(-1) (group 1), or fentanyl 1 microg kg(-1) and midazolam 0.04 mg kg(-1) (group 2), or fentanyl 1 microg kg(-1), midazolam 0.04 mg kg(-1) and lidocaine 1.5 mg kg(-1) (group 3) or fentanyl 1 microg kg(-1) (group 4) 2 min before induction of anaesthesia. Anaesthesia was established with propofol infused at 33.3 mg min(-1). RESULTS: Patients who were given midazolam required significantly less propofol to achieve satisfactory laryngeal mask insertion, median propofol doses: group 1, 1.63 mg kg(-1); group 2, 1.16 mg kg(-1); group 3, 1.01 mg kg(-1); group 4, 1.9 mg kg(-1), P < 0.0001 (analysis of variance). Patients given midazolam reported less pain on injection with propofol 13% and 3% groups (2 and 3) compared with 37.5% and 77% (groups 1 and 4) P = 0.002 (chi(2)). CONCLUSIONS: Midazolam reduces the dose of propofol required for induction of anaesthesia and successful insertion of the laryngeal mask airway. There was no clinical benefit to be gained from the addition of lidocaine.     

Comparative hemodynamic study of anesthesia induction with propofol (Diprivan), thiopental, methohexital, etomidate and midazolam in patients with coronary disease

In patients undergoing cardiac surgery, the induction of anesthesia is not without risk because of specific cardiovascular effects of the anesthetic and the preoperative state of the patient. The hemodynamic effects of etomidate, midazolam, thiopental, and methohexital are well known: etomidate is an anesthetic that induces only minor cardiovascular changes; its influence on the endocrine system, however, has reduced its clinical indication. Barbiturates such as thiopental and methohexital produce negative inotropic effects in combination with an increase in heart rate and myocardial oxygen consumption; midazolam reduces pre- and afterload in patients with poor left ventricular function. Propofol, a new short-acting induction agent with good anesthetic properties, is said to diminish arterial pressure as well as myocardial oxygen consumption. METHODS: In a randomized study we investigated the hemodynamic effects of intravenous induction with propofol (2 mg/kg body wt.), thiopental (5 mg/kg), methohexital (1 mg/kg), etomidate (0.3 mg/kg), and midazolam (0.15 mg/kg) in 50 patients undergoing coronary artery bypass grafting. All patients were premedicated with flunitrazepam (0.03 mg/kg up to 2 mg) and morphine hydrochloride (0.2 mg/kg up to 15 mg) 100 min before the investigation. After 0.003 mg/kg fentanyl the patients received the induction agent in the above-mentioned dosage within 40 s followed by 0.1 mg/kg pancuronium bromide. Hemodynamic measurements were performed 1, 3, and 5 min after the end of the injection as well as 1 and 5 min after intubation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparative study of propofol with thiopental and etomidate in anesthetic induction]

Anesthetic characteristics were studied in three homogeneous groups of twenty patients ASA I who underwent intravenous anesthetic induction with propofol 2 mg/kg; thiopental 5 mg/kg; or etomidate 0.3 mg/kg. The unconsciousness time was similar in the three groups, whereas awaking time and time of response and orientation were longer after thiopental and etomidate than after propofol. Intravenous injection of the three anesthetic agents was followed by a decrease in systolic and diastolic arterial pressure. Heart rate increased after thiopental and etomidate and had only slight fluctuations after propofol. After tracheal intubation there was a significant increase in systolic and diastolic arterial pressure and heart rate in thiopental and etomidate group. These changes were minimal after propofol. The highest number of complications occurred after etomidate.     

Implantable cardioverter-defibrillator placement in patients with mild-to- moderate left ventricular dysfunction: hemodynamics and recovery profile with two different anesthetics used during deep sedation

OBJECTIVE: To compare the effects of thiopental and propofol during defibrillation threshold testing (DFT) on hemodynamics and recovery profile in patients requiring automatic internal cardioverter-defibrilator placement. DESIGN: Prospective clinical investigation. SETTING: University hospital. PARTICIPANTS: Thirty-four adult patients. INTERVENTIONS: After administration of midazolam, 0.025 mg/kg, and fentanyl, 0.5 to 1 mug/kg, surgery was performed under topical infiltration with 1% lidocaine. In group I (GI) (n = 17), patients received thiopental by slow injection and patients in group II (GII) (n = 17) received propofol before induction of ventricular fibrillation (VF). MEASUREMENTS AND MAIN RESULTS: Patients received 4.1 +/- 1.4 mg of midazolam, 114 +/- 34 mug of fentanyl, and 280 +/- 78 mg of thiopental in GI; and 4.6 +/- 1.7 mg of midazolam, 119 +/- 62 mug of fentanyl, and 147 +/- 40 mg of propofol in GII (p > 0.05). Hemodynamics did not show significant differences between the groups at any recording time. Average time needed to regain the pretest sedation level was 16.4 +/- 8.8 minutes in GI and 10.9 +/- 5.5 minutes in GII (p = 0.03). Time required to achieve a score of 10 using a modified Aldrete score was 26.4 +/- 9.3 minutes in GI and 17.4 +/- 4.9 in GII (p = 0.001). Seven patients in GII (41%) and 1 patient in GI (6%) became hypotensive after DFT (p = 0.04). CONCLUSIONS: Deepening the sedation level by slow injection of thiopental or propofol before DFT provided satisfactory conditions during brief episodes of VF. Delay in recovery of arterial pressure after DFT with propofol and delay in arousal and discharge of patients with thiopental are major disadvantages of the regimens.     

Comparison of the Effects of Etomidate, Propofol, and Thiopental on Respiratory Resistance after Tracheal Intubation

Background: Tracheal intubation frequently results in reversible bronchoconstriction. Propofol has been reported to minimize this response in healthy patients and in asthma patients, but may be unsuitable for hemodynamically unstable patients for whom etomidate may be preferable. The current study examined respiratory resistance after tracheal intubation after induction with either thiopental, etomidate, or propofol. A supratherapeutic dose of etomidate was used to test the hypothesis that the bronchoconstrictive response could be minimized by deep intravenous anesthesia.

Methods: Seventy-seven studies were conducted in 75 patients. Anesthesia was induced with either 2.5 mg/kg propofol, 0.4 mg/kg etomidate, or 5 mg/kg thiopental. Respiratory resistance was measured at 2 min after induction.

Results: Respiratory resistance at 2 min was 8.1+/-3.4 cmH sub 2 O *symbol* l sup -1 *symbol* s (mean+/-SD) for patients receiving propofol versus 11.3+/-5.3 for patients receiving etomidate and 12.3+/-7.9 for patients receiving thiopental (P less than or equal to 0.05 for propofol vs. either etomidate or thiopental).