国产注射用盐酸瑞芬太尼有效性和安全性的评价

目的 采用随机、对照、双盲、多中心的Ⅱ期临床试验,评价国产注射用盐酸瑞芬太尼的有效性和安全性。方法201名受试者分成两组:对照组使用静脉芬太尼(2.5μkg诱导,0.03μg·kg-1·min-1维持)复合吸入66％氧化亚氮麻醉,试验组使用静脉瑞芬太尼(2μg/kg诱导,0.2μ·kg-1·min-1维持)复合吸入66％氧化亚氮麻醉。药物有效性的观察指标有:手术刺激时的应激反应,如血压、心率、流泪、麻醉质量。安全性的观察指标有:血压和心率、麻黄碱、阿托品、纳洛酮、乌拉地尔的使用量、手术失血量、心电图变化、术前和术后48 h内血中ALT、AST、肌酐、尿素氮、停止麻醉到可以拔除气管导管的时间、拔除气管导管前的PETCO2或PaCO2、停止麻醉(关闭氧化亚氮)后呼唤名字可以睁眼时间、术后送往麻醉恢复室或ICU情况以及不良事件。结果 瑞芬太尼与芬太尼在本试验剂量下,药效作用相似,但镇痛作用瑞芬太尼强于芬太尼,停止输注后其作用消退快于芬太尼。结论 国产瑞芬太尼用于全麻可产生良好的镇痛作用,且具有与芬太尼相同的安全性。     

比较布托啡诺、芬太尼及芬太尼联合曲马多用于老年患者术后镇痛的临床效果

目的研究布托啡诺用于老年患者术后静脉镇痛的疗效及不良反应。方法60例择期行上腹部手术的老年患者,随机均分为布托啡诺组(B组)、芬太尼组(F组)及芬太尼联合曲马多组(FT组),分别接受持续静脉镇痛。记录并比较术后48h内疼痛视觉模拟评分(VAS)、Ramsay镇静评分及不良反应。结果三组术后镇痛效果VAS组内比较差异无统计学意义。但术后6hF组和B组的VAS明显低于FT组(P<0.05);术后12h,B组的VAS仍低于FT组(P<0.05)。B组术后0.5、6、12h Ramsay镇静评分明显高于F组(P<0.05)。B组恶心呕吐发生率明显低于FT组(P<0.05)。结论布托啡诺可用于老年患者术后静脉镇痛。     

术毕应用芬太尼对丙泊酚-雷米芬太尼麻醉恢复的影响

目的探讨术毕应用芬太尼对丙泊酚-雷米芬太尼麻醉恢复的影响。方法45例实施腹腔镜胆囊切除术患者随机均分成F1、F1.5和F2三组,手术结束前10min分别给予芬太尼1、1.5和2μg/kg,评定拔管后疼痛和镇静程度,记录呼吸恢复、意识恢复和拔管时间以及拔管后的不良事件。结果F2组的VAS显著低于F1、F1.5组[(0.2±0.4)分vs.(2.1±1.2)分和(1.2±1.2)分](P<0.05);F2组Ramsay评分显著高于F1和F1.5组[(4.5±0.5)分vs.(3.1±0.3)分和(3.2±0.6)分](P<0.01)。F2组的呼吸恢复、意识恢复和拔管时间分别为(21.5±0.5)min,(19.5±1.5)min和(24.0±2.1)min,显著延长于F1组的(10.9±3.1)min,(12.2±3.1)min和(15.2±4.8)min和F1.5组的(11.9±3.2)min,(14.3±4.4)min和(16.7±4.5)min(P<0.01)。结论在腹腔镜胆囊切除术手术结束前10min应用1或1.5μg/kg芬太尼可减轻雷米芬太尼停药后的疼痛反应,但不显著延长苏醒和拔管时间。     

舒芬太尼或芬太尼复合丙泊酚对喉显微手术血流动力学和应激反应的影响

目的 比较芬太尼复合丙泊酚与舒芬太尼复合丙泊酚用于喉显微手术患者的血流动力学和应激激素变化.方法 200例患者行支撑喉镜下声带手术,患者随机均分为芬太尼复合丙泊酚组(F组)和舒芬太尼复合丙泊酚组(S组).F组、S组分别静脉注射芬太尼3.0μg/kg或舒芬太尼0.3μg/kg、丙泊酚2.0mg/kg、琥珀胆碱1.5mg/kg实施麻醉诱导.记录和测定两组诱导前(T0)、插管即刻(T1)、插管后1min(T2)、置支撑喉镜后1min(T3)及拔管后1min(T6)的SBP、DBP、HR、去甲肾上腺素(NE)、皮质醇(Cor)、血糖(Glu)的变化和丙泊酚用量、麻醉恢复情况及不良反应.结果 F组T1、T2、T3时SBP、DBP高于、HR快于T0和S组(P<0.05).F组T1～T3时NE、Cor、Glu分别显著高于T0和S组(P<0.05).术中丙泊酚追加量和总用药量F组显著高于S组(P<0.05),麻醉恢复时间S组稍长于F组,但差异无统计学意义.结论 舒芬太尼复合丙泊酚麻醉对血流动力学和应激反应影响小,是喉显微手术中比较理想的麻醉配伍组合.     

舒芬太尼用于手外伤术后静脉镇痛的观察

目的观察舒芬太尼用于手外伤术后静脉镇痛（PCIA）的效果。方法急诊手外伤患者78例,随机分为I组（对照组）、II组（芬太尼组）和Ⅲ组（舒芬太尼组）,每组26例。VAS评分法评估术后镇痛效果,进行术后镇静和恶心呕吐评分。结果与对照组比较,术后各时间点II组和Ⅲ组VAS评分均有显著差异（P〈0.01）,II组在术后4h、24h、48h和Ⅲ组在术后各时间点的镇静评分有显著差异（P〈0.01）,II组在术后8h的镇静评分有显著差异（P〈0.05）;与II组比较,Ⅲ组术后8h和24h的VAS评分显著降低（P〈0.05）,术后4h、12h和48hVAS评分均低于II组但差异无显著性意义,Ⅲ组术后各时间点镇静评分显著增高（P〈0.05）。Ⅲ组术后呕吐发生率明显低于II组,差异有显著性意义（P〈0.05）。结论舒芬太尼用于手外伤PCIA,镇痛确切,安全可靠,恶心呕吐发生率低于芬太尼且镇静作用强于芬太尼。     

Middle-ear pressure variations during total intravenous anesthesia with propofol, fentanyl, and ketamine

Purpose As the middle-ear cavity is one of the noncompliant gas-filled cavities, an increase in middle-ear pressure (MEP) instead of volume expansion is observed with inhalation of nitrous oxide (N₂O). Changes in MEP cause many complications, such as ear pain, temporary hearing impairment, and postoperative emesis. Therefore, we investigated changes in MEP during total intravenous anesthesia (TIVA) with propofol, fentanyl, and ketamine (PFK) and inhalation of N₂O. Methods Twelve patients were anesthetized with PFK until 60 min after the induction of anesthesia, and then N₂O (60%) inhalation was started. MEP was measured by impedance audiometry (ranging from −300 daPa to +200 daPa) at 10-min intervals during PFK, and at 2-min intervals after the inhalation of N₂O. Results MEP gradually but significantly increased from the preanesthetic value of 16±8 to 34±12 (SEM) daPa 50 min after the induction of PFK. However, MEP did not exceed the normal limit. The values of MEP in all patients were more than 200 daPa within 36 min after the start of inhalation of N₂O in oxygen. Conclusion PFK had a minimal effect on MEP, whereas addition of N₂O to PFK increased MEP dramatically. Therefore, TIVA, or at least PFK, would be a better choice for patients with middle-ear or upper-airway diseases.     

The effect of RO15-1788 on cardiovascular depression caused by fentanyl and diazepam

Cardiovascular depression occuring when diazepam is combined with fentanyl has been investigated using the benzodiazepine antagonist RO15-1788 in the dog.After the initial administration of fentanyl (40mcg/kg), the mean arterial pressure (MAP) decreased to 89% of its control value. Following the administration of diazepam (1.2mg/kg), the MAP and the total peripheral resistance (TPR) decreased significantly, to 75% and 83% of their control values respectively. After the administration of RO15-1788 (0.4mg/kg), the MAP increased significantly to 90% and the TPR to 102% of their control values and, lastly, the administration of naloxone (40mcg/kg) increased the MAP to 108% of its control value. No relationship was found between the changes in the catecholamines and the changes in the MAP after the administration of fentanyl, diazepam, and RO15-1788.The mechanism of circulatory depression when diazepam was used with fentanyl is interpreted as being a peripheral vasodilatory effect of diazepam acting by way of the benzodiazepine receptors since RO15-1788 was found to antagonize this effect.(Sone T, Kato T, Tsukahara I et al.: The effect of RO15-1788 on cardiovascular depression caused by fentanyl and diazepam. J Anesth 2: 69–76, 1988)     

Measurement of post-operative pain and narcotic administration in infants using a new clinical scoring system

We developed a clinical neurologic and behavioral scoring system composed of 10 items to measure the post-operative pain levels in infants: (1) sleep during preceeding hour, (2) facial expression of pain, (3) quality of cry, (4) spontaneous motor activity, (5) Spontaneous excitability, (6) flexion of fingers and toes, (7) sucking, (8) global evaluation of tone, (9) consolability and (10) sociability. Using this system, a group of infants ranging from one to seven months in age and undergoing minor surgical procedures was studied. The infants were randomly assigned to two groups: Group I received Fentanyl intravenously (3 g/kg) prior to surgery, and Group II received a placebo. The infants then were studied post-operatively in the recovery room at 30, 60, 90 and 120 min intervals. Over the entire post-operative observation period, 54% of the infants in Group I had satisfactory analgesia compared to 18% in Group II. There were no significant differences in Group I and Group II in oxygenation, carbon dioxide elimination, blood pressure, heart rate or temperature.     

Down-regulation of 3H-lofentanil binding to opiate receptors in different cultured neuronal cells

Summary There was stereospecific binding of ³H-lofentanil (K _D value = 1.53 nM) to membranes of neuroblastoma-glioma NG 108-15 cells which are known to bear high affinity binding sites for enkephalin derivatives (-opiate receptor subtype). There was no high affinity specific binding of the -opiate specific ligand ³H-sufentanil. The specific binding of ³H-lofentanil to -opiate receptor subtype was down-regulated (decrease in B _max value without change in the K _D value) after prolonged incubation of the cells in the presence of leu- and met- enkephalin (0.1 M). There was no down-regulation of the opiate receptors (³H-lofentanil and ³H-d-ala-d-leu-enkephalin specific binding) after incubation of NG 108-15 cells with drugs from the fentanyl series (alfentanil or sufentanil).In cultured neurones from rat forebrain (15 day old embryos), the ³H-lofentanil binding was specific with high affinity (K _D: 0.048 nM) and a slow dissociation rate similar to that in adult rat cortex. Drugs of the fentanyl series (4-anilino-piperidines) were potent displacers whereas agonists of the - (enkephalin derivatives), (phencyclidine, haloperidol, 3-hydroxyphenyl-propylpiperidine) or K- (U 50488) opiate sites had a low affinity (K _i > 0.5 M) for ³H-lofentanil specific binding sites. Since there was also specific binding of ³H-sufentanil, the opiate receptors in cultured neurones seem to be mainly of the -subtype and this is consistent with the ontogeny of opiate receptors subtypes. These receptors were down-regulated after incubation in the presence of etorphine, sufentanil and alfentanil but not enkephalin derivatives.These results strongly suggest specific binding of ³H-sufentanil and ³H-lofentanil mainly to the so-called -opiate receptors in cultured neurones and a specific binding of ³H-lofentanil to lower affinity -opiate receptors in neuroblastoma-glioma cells. The down-regulation of the -opiate binding sites in cultured neurones and that of the -site in neuroblastoma × glioma hybrid cells were dose-and temperature-dependent, induced by the corresponding high affinity agonists and prevented by naloxone. Morphine did not induce down-regulation of or receptor sites, possibly because of a partial antagonist effect on both receptor subtypes. Send offprint requests to J. M. Maloteaux at the above address