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PubMed1983

The cardiovascular effects of high-dose butorphanol-nitrous oxide anaesthesia before and during operation.

The cardiovascular effects of high doses of butorphanol (0.3-0.45 mg . kg-1) plus 60 per cent N2O anaesthesia were measured at unconsciousness, following tracheal intubation, and immediately before and at one and ten minutes after surgical stimulation in 17 A.S.A. class I and II patients undergoing elective gastric or gall bladder surgery. Butorphanol and N2O produced unconsciousness with only small decreases in heart rate and cardiac output but did not result in sufficient analgesia to block or treat stimulation of the cardiovascular system secondary to tracheal intubation or surgical incision, even when supplemented with additional butorphanol to high cumulative dose levels (1.0 mg . kg-1). The data suggest that even high dose butorphanol - N2O anaesthesia requires supplementation with other anaesthetics or anaesthetic adjuvants to prevent cardiovascular stimulation during general abdominal surgery.

Adjuvants, Anesthesia↗

PubMed1983

Evidence that nalorphine, butorphanol and oxilorphan are partial agonists at a kappa-opioid receptor.

Nalorphine, butorphanol and oxilorphan were compared in their ability to increase urinary output in the normally hydrated rat and to antagonize the increased urinary output produced by the full kappa-agonist, bremazocine. Nalorphine, butorphanol and oxilorphan increased 5-h cumulative urine output compared to controls, but the maximal effect was less than half the amount excreted after injection with 0.08 mg/kg of bremazocine. The effects of bremazocine were antagonized by nalorphine, butorphanol and oxilorphan. These effects of nalorphine, butorphanol and oxilorphan satisfy the criteria for classifying these agents as partial agonists at the kappa-opioid receptor responsible for mediating the effect of increased urinary output.

Animals↗

PubMed1989

Butorphanol precipitates abstinence in morphine dependent rats.

Butorphanol precipitated a withdrawal syndrome in rats receiving continuous intracerebroventricular infusions of morphine for three days. However, the potency of butorphanol to induce defecation, urination, teeth chattering and escape behavior was one to two orders of magnitude less on a molar basis than that of naloxone. Wet shake behavior, a prominent feature of naloxone precipitated withdrawal, was absent in morphine dependent animals challenged with butorphanol. These data indicate qualitative as well as quantitative differences in the withdrawal syndromes induced by butorphanol and naloxone.

Animals↗

PubMed1987

Butorphanol as a dental premedication in the mentally retarded.

Seventy institutionalized severely and profoundly retarded patients were administered intramuscular butorphanol, 1.0 to 4.0 mg, for premedication prior to dental procedures. These patients had been refractory to previous combined chloral hydrate and diphenhydramine treatment. Clinical efficacy was categorized according to the extent that adjunctive restraints were required to accomplish the dental procedure. A total of 151 butorphanol trials were recorded. Butorphanol was observed to be clinically effective in 74.8% of the administrations and sedation was observed in 28.2% of the trials. Dosage titration increased efficacy to 85.0%. Contribution of concurrent central nervous system depressant medication to clinical efficacy and dose requirements lacked statistical significance; however, a strong trend (p = 0.068) was found in the medication-free group with higher dosage. Vomiting (2.6%) was the most frequent adverse effect observed. One patient had marked cardiorespiratory depression that was promptly reversed by intravenous naloxone. Two patients experienced mild hypotensive episodes immediately following injection, but they recovered uneventfully. Butorphanol was shown to be a safe and effective agent for dental premedication in this difficult patient population.

Adolescent↗

PubMed1987

Comparison of butorphanol tartrate and meperidine in moderate to severe renal colic.

The analgesic efficacy and safety of parenteral butorphanol and meperidine were compared. The double-blind, randomized study involved 120 patients presenting with moderate to severe renal colic. Pain intensity and pain relief were evaluated by trained observers at fixed time intervals for four hours after study drug was administered. Eighty-three patients with documented upper urinary tract calculi were evaluated for efficacy. Butorphanol 4 mg was significantly more effective than butorphanol 2 mg and was equivalent to meperidine 80 mg. Overall efficacy assessments were "good" or "excellent" for 87 per cent, 72 per cent, and 85 per cent, respectively. There were no significant differences in side effects among treatment groups in the 83 evaluable and 27 inevaluable patients receiving study drugs. Butorphanol was effective and well-tolerated in this patient population, with important advantages over opiate analgesics.

Butorphanol↗

PubMed1982

Self-administration of nalbuphine, butorphanol and pentazocine by morphine post-addict rats.

The purpose of the study was to define possible self-administration of nalbuphine, butorphanol and pentazocine by morphine post-addict rats. Rats were prepared with permanent EEG and EMG electrodes and indwelling IV cannulae, made tolerant to and physically dependent on morphine, then trained to lever press for morphine IV self-injections on a fixed ratio (FR) 20 schedule of reinforcement. Rats were then spontaneously withdrawn from morphine. When these morphine post-addict rats were returned to the experimental cages three to four weeks later, they were found to reestablish self-administration of morphine as well as to establish self-administration of nalbuphine, butorphanol and pentazocine. Suppression of REM sleep for at least 30 min was apparent following self-injections of these agents. After the stabilization of self-injection patterns, withdrawal from nalbuphine and pentazocine was found to be associated with intense abstinence symptoms. However, withdrawal from morphine and butorphanol was not. It can be concluded that while drug-seeking behavior for the above narcotics in morphine post-addict rats was analogous as measured by self-administration, nalbuphine and butorphanol appeared to produce lower levels of physical dependence.

Animals↗

PubMed1983

The effect of peripherally administered satiety substances on feeding induced by butorphanol tartrate.

Endogenous opioid peptides appear to play a role in the initiation of feeding. Butorphanol, an exogenous opiate which preferentially generalizes to the kappa-sigma opiate receptors, is a potent initiator of feeding. In these studies, we examined the effect of peripherally administered putative satiety substances, cholecystokininoctapeptide, somatostatin, bombesin, gastrin-releasing peptide, thyrotropin-releasing hormone, calcitonin and glucagon on butorphanol induced feeding. With the exception of bombesin, all the other putative satiety factors required 2 to 32 times as high a dose to significantly suppress feeding following butorphanol compared to the dosages required to suppress starvation or tail pinch induced feeding. Bombesin appeared to be approximately equipotent in all systems tested. Haloperidol and atropine both suppressed butorphanol induced feeding supporting our previous hypothesis of an integral relationship between acetylcholinergic-dopaminergic and opioid mechanisms in the initiation of feeding. The findings reported here are compatible with an important role for opioid mechanisms in the initiation of feeding.

Acetylcholine↗

PubMed1992

Effects of beta-funaltrexamine on butorphanol dependence.

The present experiments were performed to investigate the effects of the selective mu opioid receptor antagonist, beta-funaltrexamine (beta-FNA), on the physical dependence liability of butorphanol (a mixed agonist/antagonist opioid analgesic). Butorphanol (26 nmol/microliter/h) was continuously infused via osmotic minipumps into the lateral cerebral ventricle of male Sprague-Dawley rats for 72 h. beta-FNA (12, 24, and 48 nmol/5 microliter/rat) was administered ICV 3 h prior to and 48 h after initiation of the butorphanol infusion. Treatment with beta-FNA significantly diminished naloxone-induced escape behavior, hypothermia, and loss of body weight in a dose-dependent manner, while naloxone-induced teeth-chattering, forepaw tremors, and urination were also reduced, but in a dose-independent manner. These results suggest that the mu opioid receptor is partially involved in the development of physical dependence upon butorphanol.

Animals↗

PubMed1993

Opioid antagonists and butorphanol dependence.

Butorphanol has been known to act on mu-, delta-, and kappa-opioid receptors, mu- and possibly delta-receptors are thought to mediate morphine dependence. Relative to morphine, butorphanol has a higher affinity for mu- and delta-receptors. In the present study, beta-funaltrexamine (beta-FNA) and naltrindole (NTI) (nonequilibrium mu- and delta-antagonist, respectively) were used to precipitate withdrawal in butorphanol-dependent rats. It was found that beta-FNA (12, 24, 48, and 100 nM) did not elicit significant withdrawal behaviors, while NTI caused teeth-chattering (100 nM), wet shakes (100 nM), forepaw tremors (24 nM), yawning (48 and 100 nM), ejaculation (24 nM), and urination (100 nM). The present results indicate that delta-opioid receptors may be involved in mediating butorphanol dependence, while the involvement of mu-opioid receptors needs to be further investigated.

Animals↗

PubMed1996

Transnasal butorphanol for the treatment of opioid-induced pruritus unresponsive to antihistamines.

Pruritus is a common opioid side effect and can be so severe that opioid therapy must be modified or abandoned. Antihistamines, opioid antagonists, and propofol have been proposed as treatment options, but none is universally effective. The use of intranasal butorphanol, an opioid agonist-antagonist, for pruritus has not been described previously. Six patients complaining of severe opioid-induced pruritus unresponsive to diphenhydramine received 2 mg intranasal butorphanol every 4-6 hr. Scores for pruritus, pain, and sedation were recorded on separate visual analogue scales (VAS). All patients reported significant relief from pruritus 60 min after butorphanol administration (P < 0.001); five patients noted an improvement within 15 min (P < 0.08). Sedation and pain VAS scores were not significantly different from baseline at all time points. These preliminary data demonstrate a substantial effect of intranasal butorphanol on opioid-induced pruritus that has not responded to antihistamines. Prospective controlled studies are needed to validate these findings.

Administration, Intranasal↗

PubMedDate not supplied

Epidural morphine with butorphanol in pediatric patients.

STUDY OBJECTIVE: To determine whether the addition of butorphanol to epidural morphine is effective in reducing the frequency of side effects caused by neuraxial opioids. DESIGN: Randomized, double-blind study. SETTING: Large tertiary care pediatric hospital. PATIENTS: 20 children between the ages of 2 and 17 years undergoing spinal, abdominal, or thoracic procedures. INTERVENTIONS: Patients were divided randomly into one of two groups to receive either 80 micrograms/kg of preservative-free epidural morphine (Group 1) or 80 micrograms/kg of preservative-free epidural morphine with 40 micrograms/kg of butorphanol (Group 2). MEASUREMENTS AND MAIN RESULTS: Blood pressure, heart rate, respiratory rate, and the first need for additional opioids were monitored in the two groups. In addition, pruritus, nausea and vomiting, and supplemental oxygen (O2) required to maintain oxygen saturation (SpO2) above 90% were monitored. Children who received butorphanol in addition to epidural morphine were much less likely to develop pruritus or nausea and vomiting or to require supplemental O2 to maintain SpO2 above 90%. CONCLUSION: Butorphanol 40 micrograms/kg added to epidural morphine 80 micrograms/kg is effective in decreasing the occurrence of side effects caused by neuraxial opioids in pediatric patients.

Adolescent↗

PubMed2005

Separation of enantiomers of butorphanol and cycloamine by capillary zone electrophoresis.

Butorphanol tartrate is a synthetic opioid agonist-antagonist used as analgesic, possessing three chiral centres in the basic part of the molecule. Its chiral purity is routinely controlled only by optical rotation. A new capillary zone electrophoresis method, capable to separate the enantiomers of butorphanol and intermediate of its synthesis, cycloamine, was developed. Different electrolyte composition (type and concentration of carrier ion, pH, and organic solvent addition), and type and concentration of several chiral selectors (natural and modified cyclodextrins) were tested. Using the optimized conditions (acidic electrolyte with the addition of highly sulphated gamma-cyclodextrin) as low as 0.05% of undesirable enantiomers can be detected. Selected method characteristics, i.e., linearity (0-50 mg/l), precision (2.5% at 20 mg/l), and accuracy (101 +/- 2% at 20 mg/l) were evaluated. The optimized method was applied for the analysis of real batches of butorphanol and cycloamine. It was found that butorphanol tartrate manufactured by IVAX Pharmaceuticals contains less than 0.05% of undesirable enantiomer.

Butorphanol↗

PubMed2026

Effects of detomidine alone or combined with butorphanol on oxygenation status, F-shunt and sedation level in healthy sheep.

This study evaluated the effects of detomidine alone or combined with butorphanol on arterial oxygenation, gas exchange indices, estimated shunt fraction (F-shunt) and sedation level in healthy sheep. A prospective, randomized, blinded, experimental study was conducted on twenty-seven Merino sheep allocated to three groups (9 sheep/group): 5 μg/kg detomidine +200 μg/kg butorphanol (Deto5But), 10 μg/kg detomidine + 200 μg/kg butorphanol (Deto10But), or 10 μg/kg detomidine (Deto10) administered intravenously. Following arterial and venous catheter placement, arterial blood samples were collected to determine oxygenation status and F-shunt at baseline (fraction of inspired oxygen, FiO₂: 21%), 5 min after sedation (FiO₂: 21%), and at 5 and 30 min after propofol induction (FiO₂: 100%). Sedation was evaluated by a blinded observer at 5, 10, and 15 min after drug administration using two numerical scales. Sedation produced a significant deterioration in oxygenation parameters, gas exchange indices, and F-shunt (15.36%: 95% CI 10.07-20.65; p = 0.001) compared with baseline, without significant differences between treatment groups. However, five minutes after induction of anaesthesia, the Deto5But group presented better oxygenation, gas exchange efficency, and F-shunt values compared with Deto10But (10.30%: 95% CI 0.86-19.76; p = 0.029) and Deto10 (13.93%: 95% CI 2.94-24.92%; p = 0.008). Sedation scores did not differ significantly between treatment groups or across time points. Combination of detomidine at 5 μg/kg with 200 μg/kg of butorphanol provided adequate sedation and was associated with a milder impact on oxygenation and F-shunt at 5 min post-induction.

Animals↗

PubMed2006

Subarachnoid butorphanol augments lidocaine sensory anaesthesia in calves.

To determine the efficacy and safety of subarachnoid butorphanol combined with lidocaine, six calves were studied. Each calf underwent two treatments, at least one week apart, via subarachnoid injection: (1) butorphanol (0.03 mg/kg) plus 2% lidocaine (4 mg/kg) and (2) 2% lidocaine (4 mg/kg) alone. Subarachnoid injections were performed at the lumbosacral space. Analgesia, motor block, sedation, heart rate, arterial blood pressure, respiratory rate, arterial oxygen saturation as measured by pulse oximetry, and rectal temperature were compared before and after subarachnoid administration of drugs. Subarachnoid administration of the butorphanol-lidocaine combination induced bilateral prolonged analgesia extending from the coccygeal to the T11-T13 dermatomes in the calves, with minimal sedation and severe ataxia. Cardiovascular effects were significant in both treatments: heart rate was increased, and there was a minimal decrease in arterial pressure. It was concluded that adding a small dose of butorphanol to subarachnoid lidocaine in calves is effective and safe.

Anesthetics, Local↗

PubMed1998

Supersensitivity of spinal opioid receptors to antagonists in intrathecal butorphanol and morphine dependence.

The purpose of this investigation was to evaluate changes in the sensitivity of spinal opioid receptors to selective antagonists in rats rendered dependent on intrathecal (i.t.) butorphanol and morphine. Using quantitative autoradiography, competitive binding assays with selective opioid antagonists were performed in the spinal cord sections of i.t. butorphanol- and morphine-dependent rats in which withdrawal was precipitated by i.t. naloxone. In butorphanol-dependent rats, the spinal kappa-opioid receptor developed a greater degree of antagonist supersensitivity than the spinal delta- and mu-opioid receptors did. In contrast, the spinal mu-opioid receptor became more sensitive than the delta-opioid receptor in morphine-dependent rats. These results indicate that differential supersensitivity of spinal opioid receptors was induced after chronic i.t. infusions of butorphanol and morphine.

Animals↗

PubMed1998

Differential involvement of opioid receptors in intrathecal butorphanol-induced analgesia: compared to morphine.

The present experiments were performed to investigate the differential involvement of the opioid receptor subtypes in the antinociception of intrathecal (IT) butorphanol compared to IT morphine. A single dose (26 nmol) of IT nor-binaltorphimine (nor-BNI), beta-funaltrexamine (beta-FNA), and naltrindole (NTI) demonstrated a significant attenuation in the overall antinociception of IT butorphanol (52 nmol) or IT morphine (26 nmol). However, IT butorphanol elicits thermal antinociceptive effect through kappa > delta > or = mu, whereas morphine acts on mu >delta >> kappa. These results indicate that the antinociceptive effect of both IT butorphanol and IT morphine are mediated through mu, delta, and kappa opioid receptors in different relative orders.

Analgesics, Opioid↗

PubMed2000

Influence of buprenorphine, butorphanol and nalbuphine on the initiation of intravenous cocaine self-administration in drug naive mice.

The influence of different mixed mu-kappa-opioid receptor agonists-antagonists on cocaine reinforcement was studied using the method of initiation of intravenous cocaine self-administration in naive mice. Self-administration of cocaine was readily initiated according to an inverted U-shaped unit dose-response curve. Buprenorphine, butorphanol and nalbuphine tested against the optimal unit dose of cocaine (0.8 microg per infusion), inhibited initiation of cocaine self-administration in a dose-dependent manner. When tested against a scale of cocaine unit doses (0.2 -1.6 microg per infusion) buprenorphine (0.1 mg/kg, s.c.) and nalbuphine (2 mg/kg, s. c.) produced a shift of the optimal cocaine dose from 0.8 to 0.4 microg/inf, while butorphanol (1 mg/kg, s.c.) shifted the optimal unit dose of cocaine to the right along the cocaine unit doses axis. Co-administration of naloxone (0.1 mg/kg, s.c.) significantly reduced the effect of buprenorphine but failed to influence the effect of nalbuphine and butorphanol on cocaine intake. Taken together, these results suggest that nalbuphine is capable of affecting cocaine's reinforcing properties in the same manner as buprenorphine during the initiation phase of cocaine self-administration behavior, while butorphanol causes the opposite effect. Although the exact opioid profile of action of the mixed opioid receptor agonists-antagonists is as yet not precisely known, the present findings suggest that multiple opioid receptor systems (i.e. mu and kappa) play a role in reinforcing properties of cocaine and that a co-operative interaction between mu- and kappa-opioid systems may be of importance during initiation of cocaine self-administration.

Analysis of Variance↗

PubMed1997

Caudal epidural butorphanol plus bupivacaine versus bupivacaine in pediatric outpatient genitourinary procedures.

STUDY OBJECTIVE: To investigate the efficacy of adding butorphanol to bupivacaine administered in the caudal epidural space in children undergoing genitourinary (GU) procedures. DESIGN: Randomized, double-blinded, controlled study. SETTING: University affiliated pediatric hospital. PATIENTS: 200 ASA physical status I and II male patients between 6 months and 10 years of age. INTERVENTIONS: Patients were randomized to receive either 0.25% bupivacaine with 1:200,000 epinephrine alone (Group 1) or 0.25% bupivacaine with 1:200,000 epinephrine plus 30 micrograms/kg butorphanol (Group 2) administered via the caudal epidural space prior to surgical incision. MEASUREMENTS AND MAIN RESULTS: Patients were evaluated postoperatively until discharge. Measurements included requirement of additional analgesic, sedation, pain/ comfort scores, and a 24-hour analgesic follow-up. Significantly fewer patients in the butorphanol group required rescue morphine sulfate in the postanesthesia care unit (p < or = 0.001). The total number of morphine doses administered to Group 2 was significantly less than Group 1 (p < or = 0.001). 52% of patients in Group 1 compared with 28% in Group 2 required administration of additional analgesics following discharge from the hospital (p < or = 0.003), with 23% of Group 1 requiring a codeine compound compared with 8% in Group 2 (p < 0.03). CONCLUSIONS: The addition of 30 micrograms/kg butorphanol to 0.25% bupivacaine with epinephrine via the caudal epidural space is a safe, effective means to increase duration of analgesia following GU procedures.

Ambulatory Surgical Procedures↗