瑞芬太尼对病人离体气管上皮纤毛摆动频率的影响

目的评价瑞芬太尼对病人离体气管上皮纤毛摆动频率的影响。方法择期行喉癌根治术的男性病人8例,气管造口手术中获取离体气管标本,每个标本分离出3块纤毛摆动活跃的组织块。瑞芬太尼用生理盐水稀释为0.01、8、80μg/L,每例病人的3块标本随机加入上述一种溶液,按浓度分为3组（n=8）：R0.01组、R8组、R80组。于加入瑞芬太尼前（基础值）、加入瑞芬太尼后5、10、20 min时,采用相差显微镜及成像分析技术测定气管上皮细胞纤毛摆动频率。结果与基础值比较,R8组、R80组各时点纤毛摆动频率降低（P〈0.05）。与R0.01组比较,R8组、R80组加入瑞芬太尼后各时点纤毛摆动频率均下降（P〈0.05）。结论瑞芬太尼可降低病人离体气管上皮纤毛摆动的频率。     

异丙酚效应室靶控输注与血浆靶控输注的比较

目的 观察人工流产手术使用效应室靶控输注异丙酚时的药效学变化,并与血浆靶控输注比较。方法 50例患者随机分成效应室靶控(E)和血浆靶控(B)两组,给予芬太尼1μg·kg~(-1)后分别以4μg·ml~(-1)(E组)和6μg·ml~(-1)(B组)的靶浓度输注异丙酚,观察起效时间、恢复时间、脑电频谱(BIS)值以及心率(HR)、血压(BP)、脉搏氧饱和度(SpO_2)。结果 E组起效时间及恢复时间均显著短于B组(P<0.01),而BIS值差异无显著性(P>0.05),同时E组的SpO_2显著低于B组(P<0.05)。结论 效应室靶控和血浆靶控同样适用于人工流产手术,并且起效快、恢复快,但同时应注意其呼吸抑制作用。     

丙泊酚对蟾蜍上腭纤毛摆动频率的影响

目的　了解丙泊酚对蟾蜍上腭纤毛摆动频率 (CBF)的影响。方法　取 30只中华大蟾蜍 ,每只在显微镜下将上腭粘膜分离成多个约 2mm× 2mm大小粘膜块 ,并分为四组 ,生理盐水稀释丙泊酚 ,终浓度分别为 0 0 1、1、10和 2 0 μg/ml,每组粘膜块随机加入一种浓度丙泊酚。在加入前、及加入后 5、30和 6 0min ,使用相差显微镜及成像分析技术测量纤毛上皮的CBF。结果　 0 0 1μg/ml组及 1μg/ml组 ,CBF在各时间点与基础值比均无显著差异 (P >0 0 5 ) ;10 μg/ml组和 2 0 μg/ml组 ,CBF在各时间点与基础值比 ,有显著差异 (P <0 0 5 )。各组间的CBF基础值无显著差异 (P >0 0 5 ) ;在其他时间点比较 ,丙泊酚浓度增加 ,CBF也增加 ;组间有显著差异 (P <0 0 5 )。结论　丙泊酚增加蟾蜍上腭纤毛摆动频率。     

大脑皮质功能区手术唤醒试验中异丙酚复合舒芬太尼或瑞芬太尼麻醉的效果

目的评价头皮神经阻滞、切口浸润麻醉和硬脑膜表面麻醉下,大脑皮质功能区手术唤醒试验中异丙酚复合舒芬太尼或瑞芬太尼麻醉的效果。方法择期行大脑皮质功能区手术的胶质瘤病人40例,随机分为舒芬太尼+异丙酚组(SF组,n=20)和瑞芬太尼+异丙酚组(RF组,n=20)。在头皮神经阻滞、切口浸润麻醉和硬脑膜表面麻醉下,SF组舒芬太尼血浆靶浓度为0．1～0．2 ng·ml~(-1),RF组瑞芬太尼血浆靶浓度为1～2 ng·ml~(-1),开颅期异丙酚血浆靶浓度为3～6μg·ml~(-1),唤醒期为1μg·ml~(-1)。观察循环、呼吸、颅内压的变化,计算脑灌注压,记录唤醒时间。结果两组循环稳定,术中自主呼吸,SpO_2在98％以上。呼吸暂停和呼吸抑制的发生率两组均为45％。与术前比较,两组开颅期分钟通气量下降,呼气末二氧化碳分压、颅内压升高,SF组脑灌注压降低(P＜0．05),唤醒期以上指标均恢复正常。RF组唤醒时间短于SF组(P＜0．05)。两组唤醒后镇静程度构成比比较差异无统计学意义(P＞0．05)。结论头皮神经阻滞、切口浸润麻醉和硬脑膜表面麻醉下,异丙酚复合舒芬太尼或瑞芬太尼麻醉可用于大脑皮质功能区手术唤醒试验中。     

异丙酚靶控输注靶浓度与实测浓度的差值分析及系统性能评价

目的 分析靶控输注(TCI)异丙酚靶血浆药物浓度与实测浓度的差值,评价TCI系统性能。方法 61例下腹部择期手术患者,ASA Ⅰ～Ⅱ级。微机连接佳士比3500微量泵,选用Stelpump软件内嵌Tackley药代动力学参数。恒定靶血浆药物浓度(3μg·ml~(-1)变速输注持续1h,间断采集动脉血持续1.5h。应用气相色谱-质谱(GC-MS)法测定异丙酚血浆药物浓度。结果 异丙酚输注期间各时点的实测浓度均明显高于靶浓度,停止输注后各时点的实测浓度均明显低于靶浓度(P<0.05)。输注期间TCI系统偏离度(MDPE)为30.02％、精确度(MDAPE)为31.55％、摆动度(wobble)为21.42％、分散度(divergence)为-0.51％/h。停止输注后TCI系统偏离度为19.71％、精确度为21.63％、摆动度为13.29％、分散度为-0.26％/h。结论 国人应用TCI系统输注异丙酚,其靶血浆药物浓度与实测浓度差异明显。系统偏离度和精确度均大于TCI系统性能要求的范围,摆动度偏大。     

儿童双异丙酚麻醉期的脑干听觉诱发反应

后颅凹手术常用脑干听觉诱发反应测试脑干功能。为了了解双异丙酚麻醉对儿童脑干听觉诱发反应的影响,作者选择年龄4～11岁的择期小手术患儿10例进行观察。术前1h口服异丁嗪2mg·kg~(-1)。用计算机系统控制双异丙酚输入速度,使血药浓度稳定在4μg·ml~(-1)和8μg·ml~(-1)。患儿自主呼吸,经喉罩吸入70％N_2O-O_2。用便携式NicoletV仪记录听觉诱发反应,每10s释放     

双异丙酚、阿芬太尼静注利多卡因麻醉诱导后气管插管

为了了解双异丙酚、阿芬太尼和静注利多卡因麻醉诱导气管插管条件和血流动力学反应,作者选择60例(ASAⅠ或Ⅱ级)择期施行妇科手术病人,随机等分为四组(此四组的年龄、体重、血压和心率均相仿,术前均口服替马西泮),组1静注双异丙酚2.5mg·kg~(-1),阿芬太尼10μg·kg~(-1),生理盐水5ml;组2静注双异丙酚2.5mg·kg~(-1),阿芬太尼10μg·kg~(-1),利多卡因1mg·kg~(-1);组3静注双异丙酚2.5mg·kg~(-1),阿芬太尼     

异丙酚舒张兔离体气管平滑肌的作用机制

目的 观察不同浓度的异丙酚对乙酰胆碱预处理的离体气管条的作用,并探讨其作用机制。方法 采用离体气管条模型,首先观察异丙酚在5×10-3、10-2、2.5×10-2、5×10-2和10-1mg·ml-1浓度时对乙酰胆碱预处理气管条肌张力的变化,然后分别用吲哚美辛、L-NAME、亚甲基兰、维拉帕米及格列苯脲孵育后观察上述各个浓度的异丙酚对肌张力的影响。结果 2.5×10-2、5×10-2和10-1mg·ml-1的异丙酚可使气管条舒张。用吲哚美辛、L-NAME、亚甲基兰及维拉帕米孵育后,各浓度异丙酚对肌张力的影响与未孵育时相比无明显差异(P>0.05),而用格列苯脲孵育后,可以部分阻断异丙酚舒张气管的效应(P<0.01)。结论 异丙酚的舒张离体气管平滑肌作用与前列环素、一氧化氮、胞浆可溶性鸟苷酸环化酶及电压依赖性钙通道无关,而与ATP敏感性钾通道有关。     

异丙酚对兔离体气管平滑肌细胞内游离钙离子浓度的影响

目的 评价异丙酚对兔离体气管平滑肌细胞内游离钙离子浓度([Ca2+]i)的影响.方法 采用急性酶分离方法分离兔气管平滑肌细胞,采用随机数字表法,将细胞随机分为3组(n=5):异丙酚组(Ⅰ组,终浓度300 μmol/L)、异丙酚(终浓度300 μmol/L)+2-氨乙基硼酸二苯酯(终浓度40μmol/L)(Ⅱ组)和异丙酚(300 μmol/L)+斯里兰卡肉桂碱(终浓度10 μmol/L)(Ⅲ组).Ⅰ组加入终浓度300 μmol/L的异丙酚,孵育15 min后,用无钙的Hank平衡盐溶液冲洗3次,加入1μmol/L乙酰胆碱,记录[Ca2+]i.Ⅱ组加入终浓度40μmol/L的2-氨乙基硼酸二苯酯孵育15 min后,再加入终浓度为300μmol/L的异丙酚,与2-氨乙基硼酸二苯酯共同孵育15 min后,用无钙的Hank平衡盐溶液冲洗3次,加入1 μmol/L的乙酰胆碱.Ⅲ组加入终浓度10 μmol/L的斯里兰卡肉桂碱孵育15 min后,再加入终浓度为300μmol/L的异丙酚,与斯里兰卡肉桂碱共同孵育15 min后,用无钙的Hank平衡盐溶液冲洗3次,再加入1 μmol/L的乙酰胆碱.通过负荷钙离子荧光指示剂Fluo-3/AM测定气管平滑肌细胞内[Ca2+]i.结果 与Ⅰ组比较,Ⅱ组气管平滑肌细胞内[Ca2+]i差异无统计学意义(P＞0.05),Ⅲ组[Ca2+]i明显降低(P＜0.05).结论 异丙酚可降低兔离体气管平滑肌细胞内[Ca2+]i,其机制可能与抑制内质网1,4,5-三磷酸肌醇通路有关,而与内质网兰诺定通路无关.     

在双异丙酚麻醉下用硝普钠进行控制性降压

双异丙酚麻醉时常使全身血管阻力降低,动脉血压下降,但无代偿性心率增快。为了观察该血流动力学特征对控制性降压的影响,选择24例成年患者,20～40岁,ASAⅠ～Ⅱ级,择期实施中耳手术时进行研究。术前服用安定0.2mg·kg~(-1),将患者随机分成两组,每组12例,两组均用吗啡150μg·kg~(-1)。接着Ⅰ组静注硫喷妥钠4mg·kg~(-1)和右旋筒箭毒碱0.5mg·kg~(-1),插入气管导管,吸入70％N_2O-O_2-0.6％氟烷维持麻醉。Ⅱ组静注双异丙酚2.5μg·kg~(-1),再注箭毒插气管导管,并持续静滴双异丙酚108μg·kg~(-1)·min~(-1)。麻醉维持过程中如果麻醉变浅,Ⅰ组用硫喷妥钠50mg,Ⅱ组则注双异丙酚20mg,并记录各项参数。     

七氟醚和异丙酚复合麻醉下妇科腹腔镜手术患者脑血流量和颅内压的比较

目的 比较七氟醚和异丙酚复合麻醉下妇科腹腔镜手术患者的脑血流量(CBF)和颅内压(ICP).方法 择期拟行妇科腹腔镜手术患者40例,年龄20～59岁,体重44～69kg,ASA Ⅰ或Ⅱ级,随机分为2组(n=20):七氟醚复合麻醉组(S组)和异丙酚复合麻醉组(P组).麻醉诱导:S组吸人8%七氟醚,P组TCI异丙酚(Ce 4μg/ml),两组均TCI瑞芬太尼(Ce 6ng/ml),睫毛反射消失后,静脉注射顺阿曲库铵0.15mg/kg,BIS<45时行气管插管.麻醉诱导后瑞芬太尼Ce下调为3 ng/ml,调节异丙酚Ce和七氟醚吸人浓度,维持BIS 45～50,于麻醉诱导前水平仰卧位稳定后5 min(T1)、水平截石位稳定后5 min(T2)、气管插管后即刻(T3)、气管插管后5 min(T4)、气腹头低位后即刻(T5)、气腹头低位后15 min(T6)及气腹放气后10 min(T7)时采用经颅多普勒超声测定大脑中动脉脑血流速率(CBFV)和搏动指数(PI).结果 与T1时比较,P组T3,4,7时CBFV降低,T3,4时P1降低,S组T4,7时CBFV降低,两组T5,6时PI升高(P<0.05);与T4时比较,两组T5,6时CBFV升高(P<0.05);与S组比较,P组T3时CBFV降低,T3,4时PI降低(P<0.05).结论 与七氟醚复合麻醉相比,异丙酚复合麻醉下妇科腹腔镜手术患者麻醉诱导后CBF和ICP明显降低;气腹后CBF和ICP均升高.     

Propofol stimulates ciliary motility via the nitric oxide-cyclic GMP pathway in cultured rat tracheal epithelial cells

BACKGROUND: Airway ciliary motility is impaired by inhaled anesthetics. Recent reports show that nitric oxide (NO) induces upregulation in ciliary beat frequency (CBF), and others report that propofol, an intravenous anesthetic, stimulates NO release; this raises the possibility that propofol increases CBF by stimulating the NO-cyclic guanosine monophosphate (cGMP) signal pathway. In this study, the authors investigated the effects of propofol on CBF and its relation with the NO-cGMP pathway using the pharmacologic blockers NG-monomethyl-l-arginine (l-NMMA), an NO synthase inhibitor; 1H-[1,2,4]oxidazole[4,3-a]quinoxalin-1-one (ODQ), a soluble guanylyl cyclase inhibitor; and KT5823, a cGMP-dependent protein kinase inhibitor, in cultured rat tracheal epithelial cells. METHODS: Rat tracheal tissues were explanted and cultured for 3-5 days. Images of ciliated cells were videotaped using a phase-contrast microscope. Baseline CBF and CBF 25 min after exposure to propofol or blocker were measured using video analysis. RESULTS: Vehicle (0.1% dimethyl sulfoxide; n = 11) increased CBF by 0.2 +/- 1.7% (mean +/- SD) from baseline. Propofol stimulated CBF significantly (P < 0.01) and dose dependently (1 microM, 2.0 +/- 1. 9%, n = 6; 10 microM, 8.2 +/- 6.7%, n = 9; 100 microM, 14.0 +/- 4.7%, n = 10). Intralipid (0.05%), the clinical vehicle of propofol, did not affect CBF (-0.2 +/- 2.2%; n = 5). The enhancement of CBF with use of 100 microm propofol was abolished (P < 0.01) by coadministration of 10 mmicroM l-NMMA (2.4 +/- 3.6%; n = 5), 100 microM ODQ (-0.3 +/- 2.2%; n = 6) or 30 microM KT5823 (-0.1 +/- 4. 1%; n = 8). l-NMMA, ODQ, or KT5823 alone did not change CBF. CONCLUSIONS: These results show that propofol stimulates CBF viathe NO-cGMP pathway in rat tracheal epithelial cells, suggesting a possible advantage of propofol in decreasing respiratory risk.     

Effects of propofol on extracellular acidification rates in primary cortical cell cultures: application of silicon microphysiometry to anaesthesia

Propofol depresses both cerebral oxygen consumption and glucose utilization. We tested the hypothesis that these well described effects on brain metabolism are manifest by a reduction in neuronal acid production in vitro. The rate of extracellular acidification in primary cell cultures of rat cortical neurones was measured using a novel instrument (silicon microphysiometer) after stimulation with propofol 0.3, 3 and 30 micrograms ml-1. Intralipid 10% served as a control. Propofol 3 micrograms ml-1 caused a mean decrease of 1.51 (SEM 0.71)% in baseline acidification rate, which was significantly greater than that produced by 0.3 microgram ml-1 or Intralipid alone (P < 0.05). The reduction after stimulation with propofol 30 micrograms ml-1 was 4.68 (0.35)% of baseline rates and this in turn was significantly greater than that elicited by propofol 3 or 0.3 microgram ml-1, or Intralipid (P < 0.001). We have confirmed the depressant effect of propofol on cerebral metabolism and established that propofol inhibits neuronal acid excretion in vitro.      

Differential effects of intravenous anesthetics on ciliary motility in cultured rat tracheal epithelial cells

PURPOSE: It has been shown that airway ciliary function is impaired by several anesthetic or sedative drugs, which may predispose anesthetized or intensive care patients to respiratory complications, such as hypoxemia, atelectasis and pulmonary infection. We studied the effects of midazolam, propofol, dexmedetomidine, ketamine, fentanyl, thiopental and pentobarbital on ciliary beat frequency (CBF) in isolated and cultured rat tracheal epithelial (RTE) cells, to investigate their direct CBF action removing influences of non-epithelial cells. METHODS: Rat tracheal epithelial cells were purely isolated from tracheas of adult male Sprague-Dawley rats. After 14 to 21 days of culture, the images of motile cilia were videotaped using a phase-contrast microscope. Baseline CBF and CBF 30 or 50 min after administration of vehicle or one of the above agents were computer-analyzed. RESULTS: Midazolam (0.3-10 microM), propofol (1-100 microM), dexmedetomidine (1-100 nM), fentanyl (0.1-10 nM) and thiopental (30-300 microM) had no effect on CBF. Ketamine at a supraclinical dose (1000 microM) increased CBF (22 +/- 13, mean +/- standard deviation, % increase from baseline; baseline = 100%) significantly (P < 0.01). Fentanyl at a high clinical dose (100 nM) increased CBF significantly (10 +/- 9%). Pentobarbital decreased CBF dose-dependently (100 microM, -2 +/- 6%; 300 microM, -14 +/- 18%; 1000 microM, -75 +/- 5%) and reversibly (P < 0.01). CONCLUSION: These results show that midazolam, propofol, dexmedetomidine and thiopental have no direct action on CBF in isolated RTE cells, whereas high doses of ketamine and fentanyl have direct ciliostimulatory actions and pentobarbital has a direct cilioinhibitory action.     

Coating of extracorporeal circuit with heparin does not prevent sequestration of propofol in vitro

Propofol is sequestered in extracorporeal circuits, but the factors responsible for the phenomenon are mostly unknown. We have compared two extracorporeal circuits (oxygenators, reservoirs and tubings) coated with heparin with two corresponding uncoated circuits for their capacity to sequester propofol in vitro. Three experiments were conducted with each circuit. The circuit was primed with a mixture of Ringer's acetate solution and whole blood, and the study conditions (pump flow, temperature, pH) were standardized. Propofol was added to the solution to achieve a concentration of 2 micrograms ml-1. These studies were followed with concentrations of 10- and 100-fold to assess possible saturation of propofol binding. Serial samples were obtained from the circulating solution for measurement of propofol concentration. Propofol concentrations decreased to 22-32% of the initial predicted concentration of 2 micrograms ml-1 in the circuits (no significant difference between circuits). With greater concentrations, the circuits did not become saturated with propofol, even with the highest predicted concentration of 200 micrograms ml-1. We conclude that propofol was sequestered in extracorporeal circuits in vitro, irrespective of coating the circuit with heparin.      

Propofol Stimulates Ciliary Motility via the Nitric Oxide-Cyclic GMP Pathway in Cultured Rat Tracheal Epithelial Cells

Background: Airway ciliary motility is impaired by inhaled anesthetics. Recent reports show that nitric oxide (NO) induces upregulation in ciliary beat frequency (CBF), and others report that propofol, an intravenous anesthetic, stimulates NO release; this raises the possibility that propofol increases CBF by stimulating the NO-cyclic guanosine monophosphate (cGMP) signal pathway. In this study, the authors investigated the effects of propofol on CBF and its relation with the NO-cGMP pathway using the pharmacologic blockers NG-monomethyl-l-arginine (l-NMMA), an NO synthase inhibitor; 1 H-[1,2,4]oxidazole[4,3-a]quinoxalin-1-one (ODQ), a soluble guanylyl cyclase inhibitor; and KT5823, a cGMP-dependent protein kinase inhibitor, in cultured rat tracheal epithelial cells.

Methods: Rat tracheal tissues were explanted and cultured for 3-5 days. Images of ciliated cells were videotaped using a phase-contrast microscope. Baseline CBF and CBF 25 min after exposure to propofol or blocker were measured using video analysis.

Results: Vehicle (0.1% dimethyl sulfoxide; n = 11) increased CBF by 0.2 +/- 1.7% (mean +/- SD) from baseline. Propofol stimulated CBF significantly (P < 0.01) and dose dependently (1 [mu]m, 2.0 +/- 1.9%, n = 6; 10 [mu]m, 8.2 +/- 6.7%, n = 9; 100 [mu]m, 14.0 +/- 4.7%, n = 10). Intralipid (0.05%), the clinical vehicle of propofol, did not affect CBF (-0.2 +/- 2.2%; n = 5). The enhancement of CBF with use of 100 [mu]m propofol was abolished (P < 0.01) by coadministration of 10 m[mu]m l-NMMA (2.4 +/- 3.6%; n = 5), 100 [mu]m ODQ (-0.3 +/- 2.2%; n = 6) or 30 [mu]m KT5823 (-0.1 +/- 4.1%; n = 8). l-NMMA, ODQ, or KT5823 alone did not change CBF.     

异丙酚对肝移植术患者围术期血清TNF-α、IL-6和IL-10浓度的影响

目的 探讨异丙酚对肝移植术患者围术期血清TNF-α、IL-6和IL-10浓度的影响.方法 择期原位经典肝移植术患者20例,年龄38～52岁,ASA Ⅲ级,肝功能Child评分5～11分,随机分为2组(n=10):异丙酚组(P组)于麻醉诱导后即刻静脉注射异丙酚0.5 mg/kg,然后静脉输注2 mg·ks-1·h-1至术毕;对照组(C组)给予生理盐水.于麻醉诱导后即刻(T1)、无肝期之前5 min(T2)、新肝期之前5 min(T3)、新肝期15min(T4)、新肝期60min(T5)、新肝期3 h(T6)和术后4 h(T7)时,采集静脉血3 ml,采用酶联免疫吸附法测定血清肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)和白细胞介素-10(IL-10)浓度.结果 与T1时比较,2组T2-7,时血清TNF-α、IL-6和IL-10浓度升高(P＜0.05或0.01);与C组比较,P组,T1-7时血清TNF-α和IL-6浓度降低,T4时血清IL-10浓度降低(P＜0.05或0.01).结论 异丙酚可明显抑制肝移植术患者血清TNF-α和IL-6的释放,对IL-10无影响.     

The relaxant effect of propofol on guinea pig tracheal muscle is independent of airway epithelial function and beta-adrenoceptor activity.

Airway epithelium and vascular endothelium modulate the tension of the underlying smooth muscle by releasing relaxing factors such as prostanoids and nitric oxide (NO). We investigated whether the relaxant effect of propofol on airway smooth muscle is dependent on airway epithelial function. Tracheal spirals of female guinea pigs were mounted in water-jacketed organ baths filled with Krebs-bicarbonate buffer aerated with 95% O2 and 5% CO2 at 37 degrees C. Changes in isometric tension of the specimens were measured with a force-displacement transducer and recorded with a polygraph. Propofol (10(-4) to 10(-3) M) inhibited carbachol (CCh)-, histamine (HA)-, or endothelin-1-induced contractions of the muscles in a dose-dependent manner. Neither mechanical removal of the epithelial layer, chemical inhibition of epithelial synthesis of prostanoids, nor NO affected the relaxant effect of propofol on CCh- or HA-induced tracheal contraction. Furthermore, the blockade of beta-adrenoceptors did not change the relaxant effect of propofol. These results indicate that the relaxant effect of propofol on the airway smooth muscle is independent of the epithelial function or beta-adrenoceptor activity. Propofol is an excellent anesthetic for patients with hyperreactive airways in which the epithelial layer is damaged. IMPLICATIONS: Airway epithelium, as well as vascular endothelium, plays an important role in modulating the baseline tone and reactivity of underlying smooth muscle. We investigated, in vitro, whether the relaxant effect of propofol on airway smooth muscle is dependent on airway epithelial function. We suggest that propofol relaxes airway smooth muscle independently of the epithelial function.     

Effects of target concentration infusion of propofol and tracheal intubation on QTc interval

This study was designed to evaluate the effect of target controlled infusion of propofol on QTc interval and tracheal intubation. Twenty-five unpremedicated, ASA class I or II patients were selected and target concentration infusion of propofol at 5 microg x ml(-1) was used throughout the study. The QTc interval was measured before anaesthetic induction (baseline, T1), 10 min after propofol infusion (T2), immediately after tracheal intubation (T3), and 1 min after tracheal intubation (T4). The QTc interval increased significantly at 10 min after the propofol infusion started compared to baseline (p = 0.003). After tracheal intubation, the QTc interval was further increased when compared to that at T2 (p < 0.0001). The increased QTc interval was within normal limit and no patient had an arrhythmia. In conclusion, although statistically significant, the increase in QTc interval was too small to be clinically significant during propofol infusion. However, the combination of propofol and tracheal intubation must be used carefully in patients with prolonged QTc interval.