三种不同局麻药腰麻最大运动阻滞效应的比较

目的 采用序贯试验评估罗哌卡因、左旋布比卡因和布比卡因鞘内注射后达到Bromage 3级的半数有效剂量(ED50),比较三种局麻药腰麻的运动阻滞效应.方法 腰-硬联合麻醉(CSEA)下择期行妇科手术患者99例,随机分为罗哌卡因组、左旋布比卡因组和布比卡因组,分别鞘内注射0.5%等比重罗哌卡因、左旋布比卡因或布比卡因,起始剂量均为7 mg,剂量变化梯度为1mg,鞘内注药后25 min内双下肢改良Bromage达到3级为有效.结果 罗哌卡因组腰麻产生最大运动阻滞的ED50 为9.62 mg,95%可信区间(CI)为9.16～10.09 mg;左旋布比卡因组的ED50为9.55mg,95% CI为9.01～10.11 mg;布比卡因组的ED50为6.08 mg,95% CI为5.39～6.80 mg.罗哌卡因最大运动阻滞相对效价比是布比卡因的0.63倍(95% CI 0.56～O.73).结论 罗哌卡因和左旋布比卡因腰麻的运动阻滞效应明显低于布比卡因,而罗哌卡因与左旋布比卡因无明显差异.     

妊娠对大鼠布比卡因脊麻效力的影响

目的 探讨妊娠对大鼠布比卡因脊麻效力的影响.方法 雌性SD大鼠,非孕鼠体重180～220 g,孕鼠(孕17 d)体重350～400 g.取鞘内置管成功的非孕鼠及孕鼠各18只,非孕鼠随机分为3组(n=6):正常对照组(C组)、2%布比卡因组(B2组)及4%布比卡因组(B4组);孕鼠随机分为3组(n=6):对照组(PC组)、2%布比卡因组(PB2组)及4%布比卡因组(PB4组).C组与PC组:鞘内注射生理盐水30μl,其余4组相应鞘内分别注入2%或4%布比卡因30μl.分别于给药前(基础状态)、给药后10 min、20 min、30 min、1h、2 h、4 h、1 d、2 d、3 d和4 d时测定甩尾反应潜伏期,计算最大镇痛效应百分比(MPE);并进行后肢运动功能(MF)评分.结果 与基础值比较,B2组于给药后10 min～2 h时MPE升高,给药后10 min～1 h时MF评分升高;B4组于给药后10 min～4 h时MPE升高,给药后10 min～1 h时MF评分升高;PB2组于给药后10 min～1 d时MPE升高,给药后10 min～2 h时MF评分升高;PB4组于给药后10 min～1 d时MPE升高,给药后10 min～4 h时MF评分升高(P＜0.05).结论 妊娠可增加大鼠布比卡因脊麻的效力.     

Dexmedetomidine decreases the required amount of bupivacaine for ultrasound-guided transversus abdominis plane block in pediatrics patients: a randomized study

BackgroundThe effect of dexmedetomidine on the potency of bupivacaine for transversus abdominis plane (TAP) block in pediatric patients has not been investigated.Study objectiveThe primary objective of this study was to assess the effectiveness of dexmedetomidine to decrease the concentration of bupivacaine needed for analgesia for ultrasound-guided TAP block in a pediatric patient undergoing hernia repair or hydrocelectomy.DesignThis is a randomized, double-blind, up-down, dose-finding study.SettingOperating room.PatientsSixty American Society of Anesthesiologists I and II patients aged 1-4 years scheduled for elective unilateral herniorrhaphy or hydrocelectomy.InterventionsPatients were randomly assigned to 1 of the 2 groups: group B (0.125% bupivacaine, 1 mL/kg) TAP block or group BD (0.125% bupivacaine plus 2 μg/kg dexmedetomidine, 1 mL/kg) TAP block.MeasurementsThe response of each child was observed for 60 seconds after skin incision and evaluated as ‘unsuccessful’ when skin incision caused a change in hemodynamic parameters (heart rate and mean blood pressure) 20% more than the preincision values. If the response was determined to be unsuccessful, the concentration of bupivacaine administrated to the next patient was increased by 0.02%. If it was successful, the concentration of bupivacaine administrated to the next patient was decreased by 0.02%.ResultsThe minimum local anesthetic concentration of bupivacaine was 0.0839% (0.0137) in the B group and 0.0550% (0.0169) in the BD group. The difference was statistically significant (t = 7.165, P = .0001). The total postoperative analgesic dosage of morphine was significantly higher in the B group (0.17 ± 0.04 mg/kg) than the BD group (0.11 ± 0.02 mg/kg, P = .001).ConclusionsThe addition of 2 μg/kg of dexmedetomidine reduced the minimum local anesthetic concentration of bupivacaine used for a TAP block and improved postoperative analgesia in children undergoing surgery for inguinal hernia repair or hydrocelectomy.     

Dexmedetomidine, an alpha 2-adrenoceptor agonist, reduces anesthetic requirements for patients undergoing minor gynecologic surgery

The effects of dexmedetomidine, an alpha 2-adrenoceptor agonist, on vigilance, thiopental anesthetic requirements, and the hemodynamic, catecholamine, and hormonal responses to surgery were investigated in healthy (ASA physical status 1) women scheduled for dilatation and curettage (D & C) of the uterus. Fifteen minutes before induction they received single iv doses of either dexmedetomidine (0.5 micrograms/kg; n = 19) or saline (n = 20) in a double-blind fashion. Anesthesia was induced with thiopental and maintained with N2O/O2 (70/30%) and thiopental. Dexmedetomidine was well tolerated and no serious drug-related subjective side-effects or adverse events were observed. The most prominent subjective effects were fatigue and decreased salivation. The total amount of thiopental needed to perform D & C of the uterus was reduced approximately 30% (from 456 +/- 141 mg [mean +/- SD] after saline to 316 +/- 79 mg after dexmedetomidine). This was mostly due to a smaller induction dose in the group receiving dexmedetomidine. Dexmedetomidine appeared to improve the recovery from anesthesia as measured by visual analogue scales (VAS) on fatigue and nausea. The plasma concentration of norepinephrine was decreased by 56% after dexmedetomidine implying decreased sympathetic nervous activity. Systolic and diastolic blood pressure were moderately reduced after dexmedetomidine administration. The authors conclude that dexmedetomidine preanesthetic medication decreases thiopental anesthetic requirements and improves the recuperation from anesthesia with no serious hemodynamic or other adverse effects. Further studies in patients undergoing more stressful surgery are indicated.     

Motor nerve blockade potency and toxicity of non-racemic bupivacaine in rats

BACKGROUND: Racemic [RS(+/-)] bupivacaine can be associated with severe cardiotoxicity. The S(-) isomer is known to be less neuro- and cardiotoxic, but demonstrates a lower potency to block motor activity than RS(+/-) bupivacaine. Thus, the potency and toxicity of a non-racemic bupivacaine mixture were studied. METHODS: Gastrocnemic muscle twitches induced by electrical stimulation of sciatic nerves in rats were used to compare the impact by bupivacaine solutions on motor activity. Field stimulation at 1 Hz eliciting ventricular muscle twitches was used to investigate the effects on cardiac contractility. The lethal dose of each local anesthetic agent was determined following drug infusions during general anesthesia in mechanically ventilated rats. RESULTS: Non-racemic (75S:25R) bupivacaine was more potent (P<0.05) than S(-) or R(+) enantiomers to block motor nerve activity. The concentrations of RS(+/-), 75S:25R, R(+) and S(-) bupivacaine to inhibit nerve conduction by 50% were 0.84 (0.37- 2.20), 0.84 (0.47-2.48), 2.68 (0.98-3.42) and 2.11 mM (1.5-4.03), respectively. Pronounced reductions in ventricular muscle twitches were observed with RS(+/-) and R(+) bupivacaine at low concentrations (0.5-4 microM). Lethal doses for 75S:25R (39.9 mg kg(-1)), and S(-) (34.7 mg kg(-1)) were higher (P<0.05) than for R(+) (16.2 mg kg(-1)) and RS(+/-) bupivacaine (18.4 mg kg(-1)), respectively. DISCUSSION: The potency of S(-) bupivacaine to block the motor activity in the sciatic nerve was enhanced when 25% of the S(-) isomer was replaced by the antipode R(+) bupivacaine. This effect was not associated with increased toxicity.     

Dexmedetomidine, an alpha 2-adrenergic agonist, decreases cerebral blood flow in the isoflurane-anesthetized dog

The purpose of this study was to examine the effects of dexmedetomidine, an alpha 2-adrenergic agonist, on cerebral blood flow and metabolic rate in dogs anesthetized with 0.64% isoflurane. After intubation and institution of mechanical ventilation, arterial, venous, pulmonary artery, and sagittal sinus catheters were inserted. Measurements of cerebral blood flow (CBF), cerebral metabolic rate for oxygen (CMRo2), mean arterial pressure, cardiac output, and blood gas tensions were made at various levels of isoflurane anesthesia (0.64%, 1.9%, and 2.8%), after the administration of 10 micrograms/kg of dexmedetomidine (a dose that has been shown to reduce anesthetic requirements in dogs by greater than 90%) and finally after 0.3 micrograms/kg of the alpha 2-adrenergic antagonist idazoxan. Despite an increase in arterial pressure, dexmedetomidine caused a marked reduction (greater than 45%, P less than 0.05) in CBF when compared with all preceding concentrations of isoflurane. The administration of dexmedetomidine had no effect on the CMRo2. The electroencephalogram showed a loss of high-frequency activity in a pattern similar to that seen with 1.90% isoflurane. Administration of dexmedetomidine was associated with a 57% decrease in cardiac output (to 0.89 L/min). Administration of idazoxan (an alpha 2-adrenergic antagonist) resulted in an increase in cardiac output and a reversal of the electroencephalogram effects. This experiment indicates that 10 micrograms/kg of dexmedetomidine in isoflurane-anesthetized dogs is associated with a profound decrease in CBF and cardiac output in the face of an unaltered CMRo2. Despite the large reduction in the CBF/CMRo2 ratio, there was no evidence of global cerebral ischemia.     

The effects of intrathecal levobupivacaine and bupivacaine in the elderly

The objective of this study was to compare the block durations and haemodynamic effects associated with intrathecal levobupivacaine or bupivacaine in elderly patients undergoing transurethral prostate surgery. Eighty patients were prospectively randomised to receive plain 1.5 ml levobupivacaine 0.5% (group levobupivacaine) or 1.5 ml plain bupivacaine 0.5% (group bupivacaine) in combination with fentanyl 0.3 ml (15 μg) for spinal anaesthesia. The time to reach T10 and peak sensory block level, and to maximum motor block were significantly shorter in group bupivacaine compared to group levobupivacaine (p < 0.05). Peak sensory block level was also significantly higher in group bupivacaine. In group bupivacaine, mean arterial pressure was significantly lower than group levobupivacaine, starting from 10 min until 30 min after injection (p < 0.05). Hypotension and nausea were less common in group levobupivacaine than group bupivacaine (p < 0.05). Because of the better haemodynamic stability and fewer side-effects associated with levobupivacaine, it may be preferred for spinal anaesthesia in elderly patients.     

Epidural pain relief in labour: potencies of levobupivacaine and racemic bupivacaine

We have compared the minimum local analgesic concentrations (MLAC) of levobupivacaine relative to racemic bupivacaine in a prospective, randomized, double-blind, sequential allocation study. Women in labour were given a 20-ml bolus of epidural levobupivacaine or bupivacaine diluted to a concentration determined by up-down sequential allocation. The initial concentration was 0.07% w/v for both drugs. Efficacy was defined using a visual analogue pain score (VAPS) at 10 mm or less within 30 min. The MLAC of levobupivacaine was 0.083% w/v (95% CI 0.065- 0.101) and the MLAC of bupivacaine 0.081% w/v (95% CI 0.055-0.108). In molar terms, the MLAC of levobupivacaine was 2.87 mmol litre-1 (95% CI 2.25-3.49) and the MLAC of bupivacaine 2.49 mmol litre-1 (95% CI 1.69- 3.32). With regard to the commercial preparations, the potency ratio levobupivacaine: bupivacaine was 0.98 (95% CI 0.67-1.41), and this is unlikely to be of clinical relevance. In molar terms, the ratio was 0.87 (95% CI 0.60-1.25). With regard to toxicity, the evidence should be evaluated in the light of a possible 13% potency difference in molar concentration in favour of racemic bupivacaine.      

The relative toxicity of amitriptyline,bupivacaine, and levobupivacaine administered as rapid infusions in rats

Intravascular injection of local anesthetics carries the risk of cardiovascular (CV) and central nervous system (CNS) toxicity. Amitriptyline, a tricyclic antidepressant, has local anesthetic potency that is more than that of bupivacaine. In this study, we compared the CV and CNS toxicity of the local anesthetics bupivacaine and levobupivacaine with that of amitriptyline. Twenty-nine Sprague-Dawley rats had their right external jugular vein and carotid artery cannulated under general anesthesia. On Day 2, rats were sedated with midazolam (0.375 mg/kg intraperitoneally) and received rapid infusions of either 1) bupivacaine, levobupivacaine, or amitriptyline at 2 mg x kg(-1) x min(-1) (5 mg/mL concentration) or 2) normal saline (400 micro L x kg(-1) x min(-1)) through an external jugular vein cannula. Electrocardiogram and arterial blood pressure were measured until the dose to cause impending death was reached (heart rate 50 bpm/asystole or apnea for >30 s). The mean dose required to cause apnea and impending death was significantly larger for amitriptyline (74.0 +/- 21 mg/kg and 74.5 +/- 21 mg/kg, respectively) than for levobupivacaine (32.2 +/- 20 mg/kg and 33.9 +/- 22 mg/kg, respectively) or bupivacaine (21.5 +/- 7 mg/kg and 22.7 +/- 7 mg/kg, respectively) (P < 0.05). A significantly larger dose of amitriptyline, given by rapid infusion, is required to cause CV and CNS toxicity in rats, when compared with bupivacaine and levobupivacaine. IMPLICATIONS:Amitriptyline, a tricyclic antidepressant, has local anesthetic properties and is more potent than bupivacaine. Significantly larger doses of amitriptyline, given by rapid infusion, are required to cause cardiovascular and central nervous system toxicity in rats, when compared with bupivacaine and levobupivacaine.     

Comparative somatic and visceral antinociception and neurotoxicity of intrathecal bupivacaine, levobupivacaine, and dextrobupivacaine in rats

BACKGROUND: The current study investigated whether racemic bupivacaine and its S(-)- and R(+)-enantiomers, levobupivacaine and dextrobupivacaine, differ in somatic and visceral antinociception and neurotoxicity when administered intrathecally in rats. METHODS: In experiment 1, rats intrathecally received 15 microl saline or 0.125, 0.25, 0.5, or 1% bupivacaine, levobupivacaine, or dextrobupivacaine. The tail-flick and colorectal distension tests were performed to assess somatic and visceral antinociceptive effects, respectively, for 180 min after injection. In experiment 2, rats given 0.25% anesthetic solutions were evaluated with colorectal distension-induced response in blood pressure and heart rate. In experiment 3, four groups of rats received a 1-h infusion of saline or 2.5% bupivacaine, levobupivacaine, or dextrobupivacaine. Additional rats received either 1.25% bupivacaine or levobupivacaine for 1 h. Four days after infusion, animals were assessed for persistent sensory impairment using the tail-flick test. Spinal cords and nerve roots were obtained for histologic analysis. RESULTS: In experiment 1, the three drugs produced similar time course effects and dose-effect relations in tail-flick latency. Colorectal distension thresholds and motor paralysis were slightly lower and less apparent, respectively, at some concentrations in rats given levobupivacaine than in those given the other agents. In experiment 2, colorectal distension-induced response in heart rate was less depressed in rats given levobupivacaine than in those given the other anesthetics. In experiment 3, three groups of rats given 2.5% anesthetic solutions developed similar significant increases in tail-flick latency and incurred similar morphologic damage. Two groups of rats receiving 1.25% anesthetic solutions were similar in functional impairment and nerve injury scores. CONCLUSIONS: The results suggest that, when administered intrathecally in rats, bupivacaine and its R(+)- and S(-)-enantiomers are similar for somatic antinociception and neurotoxicity but slightly different in visceral antinociception and motor paralysis, in which levobupivacaine is less potent than the others.     

左旋布比卡因与布比卡因在臂丛神经阻滞中的药效学比较

目的比较左旋布比卡因与布比卡因在臂丛神经阻滞中的药效学特性.方法60例上肢手术患者,ASA Ⅰ～Ⅱ级,随机分成三组,Ⅰ组为0.375%布比卡因,Ⅱ组为0.375%左旋布比卡因,Ⅲ组为0.375%左旋布比卡因加1：200 000肾上腺素.肌间沟法行臂丛神经阻滞.观察阻滞起效时间及持续时间、神经阻滞节段数、术中镇痛质量、不良反应以及注药前、注药后5、10、30、60 min时心率（HR）和平均动脉压（MAP）.结果Ⅱ、Ⅲ组麻醉起效时间短于Ⅰ组（P＜0.05）;麻醉持续时间Ⅱ、Ⅲ组长于Ⅰ组但差异无显著性,Ⅱ、Ⅲ组间比较差异无显著性;各组阻滞节段数、术中牵拉痛发生率、HR及MAP差异无显著性;Ⅰ组寒战发生率高于Ⅱ、Ⅲ组（P＜0.05）.结论左旋布比卡因有与布比卡因相似的药效学特性,可安全用于临床臂丛神经阻滞;肾上腺素不延长左旋布比卡因的麻醉持续时间.     

Effect of lipid emulsion on the central nervous system and cardiac toxicity of bupivacaine and levobupivacaine in awake rats

Purpose

Despite numerous studies examining the effect of lipid emulsion on bupivacaine-induced cardiac toxicity, few studies have examined its effect on central nervous system (CNS) toxicity of local anesthetics. We investigated the effect of lipid emulsion on the CNS and cardiac toxicity of bupivacaine and levobupivacaine in awake, spontaneously breathing rats.

Methods

Male Sprague–Dawley rats were randomly allocated to control–bupivacaine (CB), control–levobupivacaine (CL), lipid–bupivacaine (LB), and lipid–levobupivacaine (LL) groups (n = 8 in each group). After infusion of saline (CB and CL groups) or 20 % lipid emulsion (LB and LL groups) for 5 min, bupivacaine (CB and LB groups) or levobupivacaine (CL and LL groups) was administered IV at 1 mg/kg/min. Cumulative dose of anesthetics and their plasma concentrations at the onset of convulsions and cardiac arrest were measured.

Results

The doses of bupivacaine for inducing convulsions and cardiac arrest in the LB group (8.8 ± 1.7 and 10.2 ± 1.5 mg/kg, respectively) were significantly larger than those in the CB group (5.9 ± 1.1 and 7.1 ± 1.3 mg/kg, respectively, p < 0.001 for both). The doses of levobupivacaine for inducing convulsions and cardiac arrest in the LL group (10.0 ± 2.0 and 13.7 ± 3.6 mg/kg, respectively) were significantly larger than those in the CL group (7.7 ± 1.6 and 9.4 ± 2.4 mg/kg, p = 0.03 and p = 0.02, respectively). Plasma concentrations of bupivacaine at the onset of convulsions and cardiac arrest in the LB group (12.9 ± 2.9 and 41.4 ± 5.2 μg/ml, respectively) were significantly higher than those in the CB group (7.9 ± 1.2 and 21.6 ± 3.3 μg/ml, respectively, p < 0.001 for both). Plasma concentrations of levobupivacaine at the onset of convulsions and cardiac arrest in the LL group (17.5 ± 1.5 and 47.6 ± 6.1 μg/ml, respectively) were significantly higher than in the CL group (10.9 ± 2.2 and 29.2 ± 3.5 μg/ml, respectively, p < 0.001 for both).

Conclusions

Lipid emulsion decreased CNS and cardiac toxicity of both bupivacaine and levobupivacaine.     

Dexmedetomidine diminishes halothane anesthetic requirements in rats through a postsynaptic alpha 2 adrenergic receptor

The effect of 4(5)-[1-(2,3-dimethylphenyl)ethyl]imidazole (medetomidine), the alpha 2 adrenergic agonist, on anesthetic requirements was investigated in rats anesthetized with halothane. Halothane MAC was determined before and after either dexmedetomidine (d-enantiomer) or levomedetomidine (l-enantiomer) 10, 30, and 100 micrograms/kg or vehicle ip. There was a dose-dependent decrease in MAC with the d-, but not the l-, stereoisomer. At the highest dose of dexmedetomidine (100 micrograms/kg), halothane could be discontinued for up to 30 min with no response to tail clamping. To determine whether alpha 2 adrenoreceptors mediated this effect of dexmedetomidine on MAC, cohorts of rats were pretreated with idazoxan, 10 mg/kg ip, a highly selective alpha 2 antagonist. This completely prevented the reduction of MAC caused by dexmedetomidine. To determine whether the reduction of MAC caused by dexmedetomidine was mediated in part through either opiate or adenosine receptors, groups of rats were pretreated with either naltrexone, 5 mg/kg ip, an opiate antagonist, or 8-phenyltheophylline, 2.5 mg/kg ip, an A1 adenosine antagonist. These two pretreatments did not alter the reduction of MAC by dexmedetomidine. To determine whether postsynaptic mechanisms mediate the anesthetic effect of dexmedetomidine, rats were depleted of central catecholamine stores with either n-(2-chloroethyl)-n-ethyl-2-bromobenzylamine (DSP-4) or reserpine and alpha-methyl-para-tyrosine and MAC was determined before and after each dose of dexmedetomidine. While the catecholamine-depleted rats had a lower basal MAC than the vehicle controls, there was still a profound reduction in halothane MAC after administration of dexmedetomidine. The reduction of MAC by dexmedetomidine was blocked with idazoxan in the catecholamine depleted rats.(ABSTRACT TRUNCATED AT 250 WORDS)     

Efficacy of ropivacaine, bupivacaine, and levobupivacaine for labor epidural analgesia

STUDY OBJECTIVE: To compare analgesic efficacy and intensity of motor block with continuous infusions of ropivacaine, bupivacaine, and levobupivacaine in combination with fentanyl for labor epidural analgesia. DESIGN: Prospective, randomized, double-blinded study. SETTING: Labor and delivery suite at Magee Womens Hospital, Pittsburgh, PA. PATIENTS: 162 ASA physical status I and II, full-term, primiparous women. INTERVENTIONS: All patients received epidural labor analgesia. Epidural medication consisted of an initial bolus of 8 mL local anesthetic with fentanyl (100 microg) followed by an infusion at 12 mL/h of local anesthetic with 2 microg/mL fentanyl. Patients were allocated to one of three groups, as follows: group 1 received bolus and infusion of bupivacaine 0.125%, group 2 received bolus and infusion of levobupivacaine 0.125%, and group 3 received a bolus of ropivacaine 0.2% and infusion of ropivacaine 0.1%. MEASUREMENTS: Maternal vital signs, pain visual analog scale (VAS) score, sensory levels, and motor block (Bromage score) were recorded every hour. Duration of first and second stage of labor and mode of delivery were also recorded. RESULTS: There were no statistically significant differences in pain VAS or Bromage motor scores among the three groups of patients at any of the measured time intervals. The time to achieve T10 sensory level and patient comfort was shorter in the ropivacaine (9.35 +/- 4.96 min) and levobupivacaine (9.56 +/- 4.71 min) groups than the bupivacaine (11.89 +/- 7.76 min) group, although this difference did not reach a statistically significant level (P = 0.06). The second stage was significantly shorter in the bupivacaine group, lasting 81.27 +/- 63.3 min, compared with the ropivacaine group (121.69 +/- 86.5 min) and the levobupivacaine (115.5 +/- 83.6 minutes) group (P = 0.04). CONCLUSION: There are no significant differences in pain VAS and Bromage scores between 0.1% ropivacaine, 0.125% bupivacaine, and 0.1% levobupivacaine given for labor epidural analgesia.     

罗哌卡因、左旋布比卡因与布比卡因低位硬膜外麻醉的比较

目的比较罗哌卡因、左旋布比卡因与布比卡因低位硬膜外麻醉的临床效果。方法60例行下腹部手术病人。随机分成三组,每组20例。Ⅰ组：0．5％罗哌卡因;Ⅱ组：0．5％左旋布比卡因;Ⅲ组：0．5％布比卡因。行连续低位硬膜外麻醉。观察感觉阻滞起效时间、感觉阻滞平面上界、运动阻滞起效时间、运动阻滞程度及麻醉质量。结果Ⅰ、Ⅱ和Ⅲ组首次局麻药用量分别为（14．38±1．57）、（14．75±0．50）和（13．80±1．30）ml。Ⅰ组运动阻滞起效时间比Ⅲ组长（P〈0．05）,Ⅰ组Bromage评分为1分的例数多于Ⅲ组（P〈0．05）。与Ⅲ组比较,Ⅰ、Ⅱ组感觉阻滞起效时间、感觉阻滞平面上界差异均无统计学意义。Ⅲ组SBP在感觉阻滞平面达上界及运动阻滞起效时有明显降低（P〈0．05）。结论0．5％罗哌旨因、左旋布比卡因或布比卡因连续硬膜外麻醉均可产生良好的感觉和运动阻滞,三种药物药效学相似。     

The relative motor blocking potencies of bupivacaine and levobupivacaine in labor

Minimum local analgesic concentrations (MLAC) have been used to determine the epidural analgesic potencies of bupivacaine and its levo- counterpart. There are no reports of the motor blocking potencies of these drugs. In this study we sought to determine the motor block MLAC of both drugs and determine the relative potency ratio. Sixty ASA physical status I-II parturients were randomized. The first woman in each group received 0.25% wt/vol. Up-down sequential allocation was used to determine subsequent concentrations at a testing interval of 0.025% wt/vol. Effective motor block was defined as a Bromage score <4 within 30 min. The up-down sequences were analyzed with the Dixon and Massey method and probit regression. Two-sided P < 0.05 defined significance. The motor block MLAC for bupivacaine was 0.27% wt/vol (95% confidence interval [CI], 0.25-0.30) and for levobupivacaine was 0.31% wt/vol (95% CI, 0.29-0.34) (P = 0.024), with a levobupivacaine/bupivacaine potency ratio of 0.87 (95% CI, 0.77-0.98). This is the first study to estimate the motor-blocking potency ratio of bupivacaine and levobupivacaine in labor. This study demonstrates that the S-enantiomer of bupivacaine is less potent at motor block than the racemate. IMPLICATIONS: We estimated the motor-blocking potency ratio of bupivacaine and levobupivacaine in labor and demonstrated that the S-enantiomer of bupivacaine is less potent at motor block than the racemate.     

Spinal anesthesia: comparison of plain ropivacaine, bupivacaine and levobupivacaine for lower abdominal surgery

This study was performed to compare the anesthetic efficacy and safety of three local anesthetic agents: racemic bupivacaine and its two isomers: ropivacaine and levobupivacaine, in patients undergoing lower abdominal surgery. One hundred-twenty patients, ASA I-III, were randomized to receive an intrathecal injection of one of three local anesthetic solutions. Group A (n = 40) received 3 ml of isobaric bupivacaine 5 mg/ml (15 mg). Group B (n = 40) received 3 ml of isobaric ropivacaine 5 mg/ml (15 mg). Group C (n = 40) received 3 ml of isobaric levobupivacaine 5 mg/ml (15 mg). The onset and duration of sensory block at dermatome level T8, maximum upper spread of sensory block, time for 2-segment regression of sensory block as well as the onset, intensity and duration of motor block were recorded, as were any adverse effects, such as bradycardia, hypotension, hypoxia, tremor, nausea and/or vomiting. Time to unassisted standing up and voluntary micturition was also recorded. The onset of motor block was significantly faster in the bupivacaine group compared with that in the ropivacaine group and almost the same of that in the levobupivacaine group (P < 0.05). Ropivacaine presented a shorter duration of both motor and sensory block than bupivacaine and levobupivacaine (P < 0.05). Bupivacaine required more often the use of a vasoactive drug (ephedrine) compared to both ropivacaine and levobupivacaine and of a sympathomimetic drug (atropine) compared to the ropivacaine group.     

The influence of 2-chloroprocaine on the subsequent analgesic potency of bupivacaine

Isolated rat sciatic nerves were used to study the interaction between 2-chloroprocaine (2-CP) and bupivacaine (BP). Five nerves studied as controls were treated with 5 X 10(-4) M BP and the amplitude of the compound action potential (CAP) evoked by suprathreshold stimulation was measured. This concentration of BP completely blocked nerve conduction; but, following washout with normal Krebs-Ringer solution, the CAP amplitude recovered to 50% of initial values in 50 (+/- 4) min with a rate of recovery of 1.7 (+/- 0.6) %/min. In another series of experiments, five nerves were blocked first with 5 X 10(-4) M 2-CP, allowed to fully recover, and then were blocked with BP under the same conditions as the controls. Under these conditions, the half time for the recovery of CAP amplitude following BP was shortened to 25 (+/- 5) min, with a rate of recovery of 2.8 (+/- 0.3) %/min. When five nerves were exposed to a 5 X 10(-4) M solution of a 2-CP metabolite, 4-amino-2-chlorobenzoic acid, no nerve blockade was produced. When these nerves subsequently were blocked with BP, recovery to 50% of initial values occurred in 22 (+/- 5) min, with a rate of recovery of 2.0 (+/- 0.2) %/min. Although pretreatment with either 2-CP or 4-amino-2-chlorobenzoic acid significantly shortened the duration of BP-induced nerve blockade, neither drug had a significant effect on the rate of recovery once the CAP amplitude returned to measurable values.     

The P-glycoprotein inhibitor quinidine decreases the threshold for bupivacaine-induced, but not lidocaine-induced, convulsions in rats

PURPOSE: To examine whether inhibition of P-glycoprotein (P-gp) activity by quinidine affects the central nervous system toxicity of lidocaine and racemic bupivacaine (bupivacaine). METHODS: Forty male Sprague-Dawley rats were randomly divided into four groups (n = 10). Fifteen minutes following administration of 15 mg x kg(-1) of quinidine (QL and QB groups) or saline (L and B groups), lidocaine (L and QL groups, 4 mg x kg(-1) x min(-1)) or bupivacaine (B and QB groups, 1 mg x kg(-1) x min(-1)) was infused until convulsions occurred. Concentrations of lidocaine and its primary metabolite, monoethylglycinexylidide (MEGX) and bupivacaine in plasma and in the brain at the onset of convulsions were measured by high-performance liquid chromatography. RESULTS: There were no differences in the dose of lidocaine required to induce convulsions between the L and QL groups. There were no differences in the concentrations of total (L = 17.2 +/- 3.5, QL = 16.6 +/- 2.6 micro g x mL(-1)) or unbound lidocaine (L = 7.8 +/- 2.5, QL = 7.3 +/- 2.3 micro g x mL(-1)), total (L = 1.2 +/- 0.5, QL = 1.3 +/- 0.7 micro g x mL(-1)) or unbound MEGX (L = 0.9 +/- 0.5, QL = 0.8 +/- 0.4 micro g x mL(-1)) in plasma, total lidocaine or MEGX in the brain at the onset of convulsions between the L and QL groups. The dose of bupivacaine required to induce convulsions was comparable in the B and QB groups. At the onset of convulsions, plasma concentrations of both total (B = 4.9 +/- 1.1, QB = 4.0 +/- 0.6 micro g x mL(-1), P = 0.03) and unbound bupivacaine (B = 1.4 +/- 0.6, QB = 0.9 +/- 0.2 micro g x mL(-1), P = 0.02) were significantly lower in the QB group than in the B group. There were no differences in concentration of total bupivacaine in the brain between the B and QB groups. CONCLUSION: These results suggest that quinidine inhibited P-gp activity, resulting in increased brain/plasma concentration ratio of bupivacaine, but not of lidocaine, and decreased the threshold of plasma concentration for bupivacaine-induced convulsions.