Pre-anesthetic use of butorphanol for the prevention of emergence agitation in thoracic surgery: A multicenter, randomized controlled trial
Tao MengXiaowen LinXiming LiFangli YueYuzhu ZhangYingbin WangJianhua GuZaiqi YangHongli YuKun LvShengyong LiangXingda LiZhu WeiboGang YuTao LiYujia RenYandong LiJianjun XuWeimin XuShu WangJianbo Wu
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Background Emergence agitation (EA) is common in patients after general anesthesia (GA) and is associated with poor outcomes. Patients with thoracic surgery have a higher incidence of EA compared with other surgery. This study aimed to investigate the impact of pre-anesthetic butorphanol infusion on the incidence of EA in patients undergoing thoracic surgery with GA. Materials and methods This prospective randomized controlled trial (RCT) was conducted in 20 tertiary hospitals in China. A total of 668 patients undergoing elective video-assisted thoracoscopic lobectomy/segmentectomy for lung cancer were assessed for eligibility, and 620 patients were enrolled. In total, 296 patients who received butorphanol and 306 control patients were included in the intention-to-treat analysis. Patients in the intervention group received butorphanol 0.02 mg/kg 15 min before induction of anesthesia. Patients in the control group received volume-matched normal saline in the same schedule. The primary outcome was the incidence of EA after 5 min of extubation, and EA was evaluated using the Riker Sedation-Agitation Scale (RSAS). The incidence of EA was determined by the chi-square test, with a significance of P < 0.05. Results In total, 296 patients who received butorphanol and 306 control patients were included in the intention-to-treat analysis. The incidence of EA 5 min after extubation was lower with butorphanol treatment: 9.8% (29 of 296) vs. 24.5% (75 of 306) in the control group ( P = 0.0001). Patients who received butorphanol had a lower incidence of drug-related complications (including injecting propofol pain and coughing with sufentanil): 112 of 296 vs. 199 of 306 in the control group ( P = 0.001) and 3 of 296 vs. 35 of 306 in the control group ( P = 0.0001). Conclusion The pre-anesthetic administration of butorphanol reduced the incidence of EA after thoracic surgery under GA. Clinical trial registration [ http://www.chictr.org.cn/showproj.aspx?proj=42684 ], identifier [ChiCTR1900025705].Keywords:
Butorphanol
A double-blind, randomized trial was conducted in 120 post-surgical patients to evaluate the oral analgesic activity of butorphanol tartrate (4 mg and 8 mg) and pentazocine HCl (50 mg) as compared to placebo. Both doses of butorphanol as well as pentazocine proved to be significantly (p <0.05) more effective than placebo. Butorphanol 4 mg and pentazocine 50 mg were never significantly different from each other, while butorphanol 8 mg was significantly better than both butorphanol 4 mg as well as pentazocine 50 mg in several instances, demonstrating a significant dose effect relationship for butorphanol. All of the active treatments provided maximum pain relief within 1 to 2 hours and were effective over 4 hours. In contrast to the other treatments, none of the 8 mg butorphanol patients required remedication during the 4-hour observation period. Generally, the incidence of side-effects appeared low.
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The use of general anesthesia in dromedary camels is constrained by risks related to decubitus. Caudal epidural analgesia is an alternative convenient technique providing loco-regional analgesia for numerous invasive and noninvasive painful conditions. Lidocaine is probably the most commonly used local anesthetic in clinical practice, but has a relatively short duration and may not provide significant long term analgesic benefits. Epidural administration of an opioid-local anesthetic mixture would improve the quality and length of analgesia and minimizes the adverse motor effects provoked by local anesthetics. Butorphanol (potent agonist-antagonist opioid) has been used to improve the duration of epidural analgesia in some animal species, but not in camels. Therefore, our purpose was to investigate the onset and duration of analgesia as well as the clinical and hemato-biochemical effects produced by the epidural administration of butorphanol (0.04 mg/kg), lidocaine (0.22 mg/ kg), and butorphanol-lidocaine (0.04 mg/kg-0.22 mg/ kg) mixture in nine adult dromedary camels in a crossover experimental study.The onset of analgesia was not statistically different between lidocaine (6.5 ± 2.3 min) and butorphanol-lidocaine (7.3 ± 1.5 min) combination. Delayed onset of analgesia was reported after butorphanol administration (14.7 ± 3.5 min). Butorphanol-lidocaine combination produced marked longer duration (175 ± 8.7 min) than lidocaine (55 ± 6.8 min) and butorphanol (158 ± 5.3 min). Mild ataxia was observed in the butorphanol-lidocaine and lidocaine treated animals and slight sedation was reported after butorphanol and butorphanol-lidocaine administration. A transient significant increase in the glucose levels was recorded after all treatments.Epidural administration of butorphanol augments the analgesic effects and duration of lidocaine with minimal adverse effects.
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Enhancing effect of an opiate agonist-antagonist butorphanol (0.2 mg/kg) on sedation induced by medetomidine (80 μg/kg) was evaluated in pigs. Butorphanol significantly enhanced the depth of medetomidine-induced sedation and prolonged the duration of that assessed by posture score and spontaneous movement of pigs. The combination of medetomidine and butorphanol produced excellent muscle relaxation and moderate surface analgesia which was enough for procedures with mild pain in pigs.
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Objective
To evaluate the safety and efficacy of PCIA in the postoperative analgesic with oxycodone combined with butorphanol after thoracic surgery.
Methods
Patients received pulmonary obectomy under thoracoscope were divided into butorphanol group (164 cases) and combined group (194 cases) according to the kind of PCIA. Patients received postoperative analgesia with butorphanol only in the butorphanol group, while butorphanol and oxycodone in the combined group. VAS, times of press, total volume,Ramsay score and adverse reactions were recorded at each time points and time intervals after operation.
Results
VAS at rest was significantly lower at 6 and 24 h after the operation in the combined group than that in the butorphanol group (P<0.05). VAS during movement was lower at 24 h after the operation in the combined group (P<0.05). The times of press were lower during 6-8 h and 24-26 h after the operation in the combined group than those in the butorphanol group (P<0.05). The percentage of Ramsay score 3 was lower in combined group (P<0.05).
Conclusion
The efficacy of oxycodone combined with butorphanol is superior to butorphanol only in the intravenous patient-controlled analgesic after thoracic operation, with fewer adverse effects.
Key words:
Oxycodone; Butorphanol; Thoracic procedures; Pain, post-operative; Analgesia, patient-controlled
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Two agonist/antagonist analgesics, butorphanol tartrate (test) and pentazocine hydrochloride (standard), were compared in volunteer informed patients experiencing postoperative wound pain. The relative potency (p) is 0.04 (1 mg butorphanol equals 24.3 mg of pentazocine lactate) with upper and lower confidence limits of 0.01 and 0.07 respectively. Butorphanol tartrate in the higher dose appears to have longer duration of effect. The side effects were comparable in the population studied.
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Abstract Butorphanol is a synthetic opioid agonist/antagonist analgesic agent that mainly exerts its effects through κ‐opioid receptors. It has been demonstrated that κ‐opioid receptors preferentially mediate the development of physical dependence upon butorphanol and the associated withdrawal syndrome. However, it is not fully understood whether or not nNOS‐containing neurons in the various brain regions play an important role in butorphanol withdrawal. Therefore, this study was conducted to determine whether the selective nNOS inhibitor, 7‐NI, modifies the development of butorphanol withdrawal and changes of nNOS expressions in different brain regions in physically butorphanol‐dependent rats. The first part of the study focused on withdrawal behaviors in male Sprague‐Dawley rats. Physical dependence was induced by a 72‐h i.c.v. infusion with butorphanol (26 nmol/μl/h) and withdrawal was subsequently precipitated by i.c.v. challenge with naloxone (48 nmol/5 μl/rat) 2 h after termination of the butorphanol infusion. The butorphanol/7‐NI coadministration group showed a significant decrease in several signs of withdrawal such as teeth chattering, as compared with the butorphanol‐treated group. In the second part of the study, immunohistochemical analysis was performed to determine the expression of nNOS in the various brain regions. In the butorphanol/7‐NI coadministration group, the number of cells labeled for nNOS was significantly lower in the various brain regions (including the caudate putamen, nucleus accumbens, and hippocampus) than in the butorphanol group. Therefore, 7‐NI decreased in butorphanol‐induced physical dependence and nNOS expression. Taken together, these findings suggest that the nNOS system is involved in the development of butorphanol‐induced physical dependence, and 7‐NI has potential clinical application as a candidate for the treatment of opioid withdrawal syndrome. Synapse 62:582–589, 2008. © 2008 Wiley‐Liss, Inc.
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The effects of butorphanol were studied in assays of antinociception, respiratory depression, sedation, diuresis and reinforcing effects in rhesus monkeys, and opioid binding in monkey brain. Butorphanol (0.003-0.1 mg/kg s.c.) was effective in the warm-water tail withdrawal assay in 50 degrees C water but not in 55 degrees C. Over a similar dose range, butorphanol caused substantial respiratory depression, without an obvious plateau. Constrained quadazocine apparent pA2 analysis on the respiratory depressant and antinociceptive effects of butorphanol yielded different values between the two assays (respiratory depression pA2 = 6.61; antinociception pA2 = 8.26). Butorphanol (0.1 mg/kg) antagonized the antinociceptive effects of etonitazene in 55 degrees C water, but caused a nonparallel leftward shift in the U50,488 dose-effect curve; both effects were probably due to butorphanol's intermediate efficacy at mu receptors. Butorphanol (0.0001-0.003 mg/kg per injection i.v.) was self-administered; unlike other mu opioid agonists, its maximum effect was depressed after pretreatment with quadazocine (0.01-1.0 mg/kg). Butorphanol (0.003-0.32 mg/kg) was devoid of substantial sedative or muscle relaxant effects, as measured by observational rating scales. Butorphanol (0.01-0.1 mg/kg s.c.), unlike U50,488 (0.01-0.32 mg/kg) did not cause diuresis. Kappa agonist or antagonist effects of butorphanol were not detected in the present studies. This profile is consistent with butorphanol's binding characteristics in rhesus monkey brain which indicated 12-fold mu:kappa selectively and 34-fold mu:delta selectivity.
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This study evaluated the effect of butorphanol tartrate, a synthetic opioid agonist-antagonist, on halothane minimum alveolar concentration (MAC) in dogs. Baseline halothane MAC was determined in each of six dogs. Butorphanol was administered and halothane MAC was redetermined. Each dog received butorphanol at 0.2, 0.4, and 0.8 mg/kg intravenously at 1 week intervals. Heart rate and arterial blood pressure decreased after butorphanol administration, but returned to baseline by 50 minutes. There was little effect on respiratory parameters. A halothane-sparing effect was not noted with any butorphanol dose.
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Abstract Objective —To determine the pharmacokinetics of butorphanol tartrate after IV and IM single-dose administration in red-tailed hawks (RTHs) and great horned owls (GHOs). Animals —6 adult RTHs and 6 adult GHOs. Procedures —Each bird received an injection of butorphanol (0.5 mg/kg) into either the right jugular vein (IVj) or the pectoral muscles in a crossover study (1-week interval between treatments). The GHOs also later received butorphanol (0.5 mg/kg) via injection into a medial metatarsal vein (IVm). During each 24-hour postinjection period, blood samples were collected from each bird; plasma butorphanol concentrations were determined via liquid chromatography-mass spectrometry. Results —2- and 1-compartment models best fit the IV and IM pharmacokinetic data, respectively, in both species. Terminal half-lives of butorphanol were 0.94 ± 0.30 hours (IVj) and 0.94 ± 0.26 hours (IM) for RTHs and 1.79 ± 1.36 hours (IVj), 1.84 ± 1.56 hours (IM), and 1.19 ± 0.34 hours (IVm) for GHOs. In GHOs, area under the curve (0 to infinity) for butorphanol after IVj or IM administration exceeded values in RTHs; GHO values after IM and IVm administration were less than those after IVj administration. Plasma butorphanol clearance was significantly more rapid in the RTHs. Bioavailability of butorphanol administered IM was 97.6 ± 33.2% (RTHs) and 88.8 ± 4.8% (GHOs). Conclusions and Clinical Relevance —In RTHs and GHOs, butorphanol was rapidly absorbed and distributed via all routes of administration; the drug's rapid terminal half-life indicated that published dosing intervals for birds may be inadequate in RTHs and GHOs.
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