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PubMed1994

Butorphanol increases food-reinforced operant responding in satiated rats.

In the present series of studies we examined the effect of butorphanol tartrate on food-reinforced operant responding in satiated rats. In the first experiment, 8.0 mg/kg butorphanol was administered subcutaneously, once per day for 4 days, to satiated rats responding under an fixed ratio 10 (FR 10) reinforcement schedule. In the second experiment, butorphanol (0, 0.3, 1.0, 3.0, 10.0 mg/kg) was administered to satiated rats responding under an FR 80 (first pellet) FR 3 (subsequent pellets) reinforcement schedule for 4 consecutive days. Repeated butorphanol administration increased total amount of food consumed over sessions in both experiments. Under the FR 80 schedule component, butorphanol initially increased latency to acquire the first pellet, an effect attenuated by repeated administration. Whereas vehicle administration was associated with consumption of relatively large quantities of food within the first 10 min of receiving the first pellet, butorphanol was associated with continued feeding as the session progressed. These data suggest that butorphanol-induced food intake is associated with maintenance rather than initiation of feeding.

Animals↗

PubMed1994

High-performance liquid chromatographic method for the quantitative determination of butorphanol, hydroxybutorphanol, and norbutorphanol in human urine using fluorescence detection.

A sensitive, quantitative reversed-phase high-performance liquid chromatographic method has been established for the simultaneous determination of butorphanol, a synthetic opioid, and its metabolites, hydroxybutorphanol and norbutorphanol, in human urine samples. The method involved extraction of butorphanol, hydroxybutorphanol, and norbutorphanol from urine (1.0 ml), buffered with 0.1 ml of 1.0 M ammonium acetate (pH 6.0), onto 1-ml Cyano Bond Elut columns. The eluent was evaporated under nitrogen and low heat, and reconstituted with the HPLC mobile phase, acetonitrile-methanol-water (20:10:70, v/v/v), containing 10 mM ammonium acetate and 10 mM TMAH (pH 5.0). The samples were chromatographed on a reversed-phase octyl 5-microns column. The analysis was accomplished by detection of the fluorescence of the three analytes, at excitation and emission wavelengths of 200 nm and 325 nm, respectively. The retention times for hydroxybutorphanol, norbutorphanol, the internal standard, and butorphanol were 5.5, 9.0, 13.0, and 23.4 min respectively. The validated quantitation range of the method was 1-100 ng/ml for butorphanol and hydroxybutorphanol, and 2-200 ng/ml for norbutorphanol in urine. The observed recoveries for butorphanol, hydroxybutorphanol, and norbutorphanol were 93%, 72%, and 50%, respectively. Standard curve correlation coefficients of 0.995 or greater were obtained during validation experiments and analysis of study samples. The method was applied on study samples from a clinical study of butorphanol, providing a pharmacokinetic profiling of butorphanol.

Butorphanol↗

PubMed1991

Interaction of butorphanol, with monoamine oxidase inhibitor, tranylcypromine.

This investigation examines the possibility of interaction between tranylcypromine and butorphanol in comparison to pethidine. The LD50 of pethidine and butorphanol were determined in mice pretreated with the non-selective monoamine oxidase (MAO) inhibitor, tranylcypromine orally for 8 days or with oral saline solution. Tranylcypromine decreased the LD50 of both pethidine and butorphanol by 78% and 41%, respectively. Anesthetized rabbits with halothane pretreated with tranylcypromine or saline were given pethidine (5 mg/kg i.v.) or butorphanol (0.5, 1 and 2 mg/kg i.v.). Pethidine produced a marked increase in blood pressure in rabbits pretreated with tranylcypromine and did not affect significantly the heart rate. Butorphanol did not affect either blood pressure or heart rate at doses of 0.5 or 1 mg/kg. However, the largest dose of butorphanol (2 mg/kg) produced hypotension and tachycardia in rabbits pretreated with tranylcypromine. Neither pethidine nor butorphanol affected the temperature of anesthetized rabbits pretreated with tranylcypromine or saline.

Animals↗

PubMed1980

Human perinatal distribution of butorphanol.

The perinatal distribution of butorphanol was demonstrated in relation to maternal-neonatal transfer and colostrum/milk excretion in obstetric patients. Parenteral butorphanol passed the placental barrier and was found in neonatal cord serum. The mean neonatal serum concentration of butorphanol was not different from the mean maternal serum concentration of butorphanol, following a 1 or 2 mg intramuscular dose. Butorphanol was detected in the milk of lactating women following oral and intramuscular administration. Serum and milk concentrations appeared to be parallel with time. This observation was confirmed by the constancy of the mean milk-to-serum concentration ratio (0.7 intramuscular, 1.9 oral). We calculated that 4 micrograms would be the maximum amount of butorphanol, which would be expected to be present in the full daily milk output (1 L) following administration four times a day of 2 mg intramuscular or of 8 mg oral doses. An oral dose of 4 micrograms to an infant weighing 4 kg corresponds to the negligible oral dose of 0.7 mg to a 70 kg adult. The demonstrated safety and efficacy of butorphanol as an obstetric analgesic and the characteristics of the maternal-neonatal transfer and milk excretion are indicative of the potential excellence of this agent for obstetric use.

Anesthesia, Obstetrical↗

PubMed1999

Autoradiographic study of NMDA-displaceable [3H]glutamate and [3H]MK-801 binding during butorphanol withdrawal in the rat brain.

Influences of continuous administration of butorphanol on the autoradiography of [3H]glutamate binding and [3H]MK-801 binding were investigated to study the effects of butorphanol withdrawal on NMDA receptors. Rats were administered butorphanol (26 nmol microl(-1) h(-1)) by continuous intracerebroventricular (i.c.v.) infusion through pre-implanted cannula connected to osmotic mini-pumps for 3 days. Rats were then sacrificed at 2, 7, and 24 h after discontinuation of butorphanol infusion. [3H]MK-801 binding was slightly increased in the cortical area, hippocampus, and cerebellum in 2, 7, and 24 h withdrawal groups and was shown most significant increase in the 7 h withdrawal group. NMDA-displaceable [3H]glutamate binding was markedly increased in the cortical area, striatum, septum, hippocampus, thalamus, and cerebellum in 7 h withdrawal group and was significantly increased in the striatum, hippocampus, and thalamus in 24 h withdrawal group. These results demonstrate that the development of butorphanol withdrawal is more prominent by 7 h after discontinuation of butorphanol infusion and suggest that NMDA binding sites at NMDA receptors may play more important role in the development of butorphanol withdrawal than that of channel blocking sites.

Animals↗

PubMed2002

Withdrawal from dependence upon butorphanol uniquely increases kappa(1)-opioid receptor binding in the rat brain.

Changes in kappa(1)-opioid receptor binding have been implicated in the development of dependence upon and withdrawal from butorphanol. Autoradiographic characterization of binding for brain kappa(1)-([3H]CI-977), mu-([3H]DAMGO), and delta-([3H]DPDPE) opioid receptors was performed in rats undergoing naloxone-precipitated withdrawal from dependence upon butorphanol or morphine. Dependence was induced by a 72h i.c.v. infusion with either butorphanol or morphine (26nmol/microl/h). Withdrawal was subsequently precipitated by i.c.v. challenge with naloxone (48 nmol/5 microl/rat), administered 2h following cessation of butorphanol or morphine infusion. During withdrawal from butorphanol, but not morphine, kappa(1)-opioid receptor binding was increased significantly in the frontal cortex, posterior basolateral amygdaloid nucleus, dorsomedial hypothalamus, hippocampus, posterior paraventricular thalamic nucleus, ventral tegmental area and locus coeruleus. In contrast, mu-opioid receptor binding decreased in these brain regions in naloxone-precipitated withdrawal from morphine, but not butorphanol, while binding for delta-opioid receptors was altered in both withdrawal groups. The brain kappa(1)-opioid receptor appears to be more directly involved in the development of physical dependence upon, and the expression of withdrawal from, butorphanol, as opposed to the prototypical opioid analgesic, morphine.

Analgesics, Opioid↗

PubMedDate not supplied

Comparison of butorphanol nasal spray and fiorinal with codeine in the treatment of migraine.

Butorphanol tartrate is a synthetic mixed agonist-antagonist opioid analgesic. Its transnasal dosage form, which may be self-administered when the use of an opioid analgesic is appropriate, was previously shown to provide rapid relief of migraine pain. In this double-blind, parallel-group, outpatient study, we compared butorphanol nasal spray 1 mg followed in 1 hour by an optional second 1-mg dose with the orally administered analgesic, Fiorinal with Codeine (one capsule containing butalbital 50 mg, caffeine 40 mg, aspirin 325 mg, and codeine phosphate 30 mg). Patients (N=321) were assigned by randomization to one of two treatment groups (butorphanol or Fiorinal with Codeine) and instructed to self-administer medication when migraine pain reached an intensity of moderate or severe and to record study-related events in a diary for 24 hours posttreatment. Efficacy analyses were performed on data from 275 patients who took study medication and returned a patient diary; 136 in the butorphanol group and 139 in the Fiorinal with Codeine group. During the first 2 hours after treatment, butorphanol was more effective than Fiorinal with Codeine in treating migraine pain as measured by pain intensity difference scores, percentage of responders (pain decreased to mild or none), percentage of pain-free patients, and degree of pain relief, with a more rapid time to onset of 15 minutes. A similar percentage of patients in the two groups used rescue medication during the first 4 hours, after which more butorphanol-treated than Fiorinal with Codeine-treated patients used rescue medication. Butorphanol patients had more side effects, less improvement in digestive symptoms, and less improvement in functional ability than Fiorinal with Codeine patients.

Administration, Intranasal↗

PubMed1998

Transnasal butorphanol is effective for postoperative pain relief in children undergoing myringotomy.

BACKGROUND: More than 70% of children require analgesics after bilateral myringotomy and tube placement (BMT). Because anesthesia for BMT is generally provided by face mask without placement of an intravenous catheter, an alternative route for analgesia administration is needed. Transnasal butorphanol is effective in relieving postoperative pain in adults and children. The effectiveness of transnasal butorphanol for postoperative pain management in children undergoing BMT was studied. METHODS: This double-blinded, placebo-controlled study compared the postoperative analgesic effects of transnasal butorphanol administered after the induction of anesthesia. Sixty children classified as American Society of Anesthesiologists physical status 1 or 2 who were aged 6 months or older and scheduled for elective BMT were randomized to receive transnasal placebo or 5, 15, or 25 microg/kg butorphanol. Postoperative pain was assessed using the Children's Hospital of Eastern Ontario Pain Scale (CHEOPS) on arrival in the postanesthesia care unit and at 5, 10, 15, 30, 45, and 60 min. RESULTS: The CHEOP scores were significantly less in the 25 microg/kg transnasal butorphanol group compared with controls. Significantly fewer children received rescue analgesia in the 25 microg/kg transnasal butorphanol group compared with controls (n = 1 and 8, respectively; P = 0.02). CONCLUSIONS: Transnasal butorphanol given in a dose of 25 microg/kg after induction of anesthesia provided adequate postoperative pain relief in children undergoing BMT.

Administration, Intranasal↗

PubMed1999

Effect of butorphanol tartrate on shock-related discomfort during internal atrial defibrillation.

BACKGROUND: In patients with atrial fibrillation, intracardiac atrial defibrillation causes discomfort. An easily applicable, short-acting analgesic and anxiolytic drug would increase acceptability of this new treatment mode. METHODS AND RESULTS: In a double-blind, placebo-controlled manner, the effect of intranasal butorphanol, an opioid, was evaluated in 47 patients with the use of a step-up internal atrial defibrillation protocol (stage I). On request, additional butorphanol was administered and the step-up protocol continued (stage II). Thereafter, if necessary, patients were intravenously sedated (stage III). After each shock, the McGill Pain Questionnaire was used to obtain a sensory (S), affective (A), evaluative (E), and total (T) pain rating index (PRI) and a visual analogue scale analyzing pain (VAS-P) and fear (VAS-F). For every patient, the slope of each pain or fear parameter against the shock number was calculated and individual slopes were averaged for the placebo and butorphanol group. All patients were cardioverted at a mean threshold of 4.4+/-3.3 J. Comparing both patient groups for stage II, the mean slopes for PRI-T (P=0.0099), PRI-S (P=0.019), and PRI-E (P=0.015) became significantly lower in the butorphanol group than in the placebo group. Comparing patients who received the same shock intensity ending stage I and going to stage II, in those patients randomized to placebo the mean VAS-P (P=0.023), PRI-T (P=0. 029), PRI-S (P=0.030), and PRI-E (P=0.023) became significantly lower after butorphanol administration. CONCLUSIONS: During a step-up internal atrial defibrillation protocol, intranasal butorphanol decreased or stabilized the value of several pain variables and did not affect fear. Of the 3 qualitative components of pain, only the affective component was not influenced by butorphanol. The PRI evaluated pain more accurately than the VAS.

Administration, Intranasal↗

PubMed1994

Epidural morphine combined with epidural or intravenous butorphanol for postoperative analgesia in pediatric patients.

We performed a prospective, randomized, double-blinded study in 60 postoperative pediatric patients aged 6 wk to 7 yr to compare the efficacy of butorphanol given epidurally or intravenously in preventing the side effects of epidural morphine. Three groups of patients received 60 micrograms/kg epidural morphine; 20 patients also received epidural butorphanol 30 micrograms/kg, and 20 patients also received 30 micrograms/kg intravenous butorphanol. All patients were evaluated for analgesia, sedation, vomiting, urinary retention, pruritus, and respiratory depression for 24 h postoperatively. Although the overall incidence of side effects was not different in the three groups, the epidural butorphanol group had a significant decrease in severity of pruritus. Sedation was seen more frequently in the groups receiving butorphanol, but was most pronounced in the epidural butorphanol group. We conclude that butorphanol has little or no effect on the side effects of epidural morphine.

Butorphanol↗

PubMed2005

Influence of medetomidine on stress-related neurohormonal and metabolic effects caused by butorphanol, fentanyl, and ketamine administration in dogs.

OBJECTIVE: To examine stress-related neurohormonal and metabolic effects of butorphanol, fentanyl, and ketamine administration alone and in combination with medetomidine in dogs. ANIMALS: 10 Beagles. PROCEDURE: 5 dogs received either butorphanol (0.1 mg/kg), fentanyl (0.01 mg/kg), or ketamine (10 mg/kg) IM in a crossover design. Another 5 dogs received either medetomidine (0.02 mg/kg) and butorphanol (0.1 mg/kg), medetomidine and fentanyl (0.01 mg/kg), medetomidine and ketamine (10 mg/kg), or medetomidine and saline (0.9% NaCI) solution (0.1 mL/kg) in a similar design. Blood samples were obtained for 6 hours following the treatments. Norepinephrine, epinephrine, cortisol, glucose, insulin, and nonesterified fatty acid concentrations were determined in plasma. RESULTS: Administration of butorphanol, fentanyl, and ketamine caused neurohormonal and metabolic changes similar to stress, including increased plasma epinephrine, cortisol, and glucose concentrations. The hyperglycemic effect of butorphanol was not significant. Ketamine caused increased norepinephrine concentration. Epinephrine concentration was correlated with glucose concentration in the butorphanol and fentanyl groups but not in the ketamine groups, suggesting an important difference between the mechanisms of the hyperglycemic effects of these drugs. Medetomidine prevented most of these effects except for hyperglycemia. Plasma glucose concentrations were lower in the combined sedation groups than in the medetomidine-saline solution group. CONCLUSIONS AND CLINICAL RELEVANCE: Opioids or ketamine used alone may cause changes in stress-related biochemical variables in plasma. Medetomidine prevented or blunted these changes. Combined sedation provided better hormonal and metabolic stability than either component alone. We recommend using medetomidine-butorphanol or medetomidine-ketamine combinations for sedation or anesthesia of systemically healthy dogs.

Analgesia↗

PubMed1988

Cardiopulmonary effects of nalbuphine hydrochloride and butorphanol tartrate in sheep.

The cardiopulmonary, sedative and analgesic effects of butorphanol tartrate and nalbuphine hydrochloride were evaluated in six adult crossbred Dorset sheep (Ovis aries). The animals were divided randomly into two groups of three. The first group received butorphanol tartrate (0.5mg/Kg s.c.) followed in 3 days by nalbuphine hydrochloride (1 mg/Kg, s.c.). The second group received nalbuphine followed in 3 days by butorphanol. Cardiopulmonary parameters were evaluated at baseline (once the animal had accommodated to restraint); immediately following analgesic administration; and at 15, 30, 60, 90 and 120 minutes after analgesic administration. No significant changes (alpha greater than .05) from baseline were seen in any of the measured cardiopulmonary parameters from either the butorphanol or nalbuphine groups. Butorphanol produced the most dramatic analgesic and sedative effects with onset of both within 15 minutes of administration and peak effects occurring 30 minutes post injection. The degree of analgesia was diminished at 120 minutes while the sedative effect returned to near baseline by 90 minutes. The nalbuphine group also showed an onset of analgesia 15 minutes post injection reaching a peak effect after 30 minutes. However, onset of sedation occurred 30 minutes post injection achieving a peak effect at 60 minutes which was markedly less than that of butorphanol. As in the butorphanol group, analgesia was diminished at 120 minutes.

Analgesia↗

PubMed1982

Antiemetic activity of butorphanol against cisplatin-induced emesis in ferrets and dogs.

The analgesic agent butorphanol was evaluated for its ability to block cisplatin-induced emesis in ferrets and dogs. In ferrets, butorphanol (0.15, 0.3, or 0.45 mg/kg; expressed in terms of the tartrate salt) administered sc 30 minutes prior to cisplatin (8 mg/kg iv) reduced the number of emetic episodes but did not eliminate them. When these doses of butorphanol were administered 30 minutes before and 30 and 90 minutes after cisplatin, they caused a dose-related reduction in the number of emetic episodes; there was complete protection at a dose of 0.45 mg/kg/injection. In dogs, butorphanol (0.185 or 0.37 mg/kg/injection, expressed in terms of the tartrate salt) was administered sc on the same multiple-dose schedule used in the ferrets; this caused a nearly complete elimination of the emetic response to cisplatin (3 mg/kg iv). Butorphanol caused some sedation in both species at effective antiemetic doses but had no effect on the antitumor activity of cisplatin against murine L1210 leukemia. Naloxone blocked the antiemetic effect of butorphanol in ferrets, indicating the involvement of opiate receptors. The results of these studies suggest that butorphanol may be useful clinically in mitigating the emetic effects of cisplatin.

Animals↗

PubMed1997

Induction of tolerance to intrathecal butorphanol in rats.

BACKGROUND: Butorphanol, an opioid agonist/antagonist, has been administered spinally and epidurally in humans for moderate to severe pain. However, unlike intrathecal (i.t.) morphine, virtually no information is available regarding butorphanol's ability to induce analgesic tolerance at the spinal cord level upon chronic i.t. administration. METHODS: Continuous infusion of i.t. butorphanol was given via an osmotic minipump. Rats were randomly assigned to four groups (n = 7 each) to receive i.t. infusion (1 microliter/h) consisting of saline, or butorphanol (13, 26, or 52 nmol/h) for 96 h. Tail-flick (TF) latencies were measured during the period of i.t. infusion. RESULTS: A dose-dependent antinociceptive effect, as measured by TF latency, was demonstrated in the groups receiving i.t. butorphanol as compared to the saline group. The overall antinociceptive effects calculated from the areas under the curve (AUC's) were 372 +/- 3.0, 394 +/- 7.5, and 433 +/- 20 for the 13, 26, and 52 nmol/h butorphanol-infused groups, respectively; the AUC's of the 26 and 52 nmol/h groups were significantly different from the AUC of 356 +/- 3.4 for the saline-infused group (p < 0.01, one way ANOVA; p < 0.05, post hoc Dunnett's test). The TF latencies of the 26 and 52 nmol/h groups were 3.77 +/- 0.05 and 3.73 +/- 0.03 s at the baseline (before the i.t. infusion), respectively; and gradually increased significantly (p < 0.01, two way repeated measure ANOVA; p < 0.05, post hoc Student-Newman-Keuls or SNK test) to the peak values of 4.31 +/- 0.14 and 4.90 +/- 0.28 s, respectively; then decreased significantly from the peaks (p < 0.05, post hoc SNK test) to the final values of 3.87 +/- 0.06 and 4.10 +/- 0.13 s at the end of the 96-h infusion, respectively. The TF values of the saline and the 13 nmol/h groups did not show statistically significant differences throughout the 96-h infusion period. CONCLUSIONS: Therefore, continuous infusion of i.t. butorphanol at the rate of 26 and 52 nmol/h induced tolerance to tail-flick analgesia within 96 h.

Analgesics, Opioid↗

PubMed1998

Evaluation of analgesia provided by postoperative administration of butorphanol to cats undergoing onychectomy.

OBJECTIVE: To evaluate adequacy of analgesia provided by postoperative administration of butorphanol to cats undergoing onychectomy. DESIGN: Randomized controlled trial. ANIMALS: 63 cats undergoing elective onychectomy. PROCEDURE: Cats were randomly assigned to a treatment (n = 42) or control group (21). Cats in the treatment group were given butorphanol parenterally immediately and 4 hours after surgery and orally for 2 days after surgery. Rectal temperature, heart rate, and respiratory rate were recorded and scores were assigned for temperament, recovery, sedation, analgesia, and lameness for the first 24 hours after surgery. Owners provided scores for appetite, personality, and lameness the first and second days after discharge from the hospital. RESULTS: Heart rate, respiratory rate, rectal temperature, and temperament and sedation scores were not significantly different between groups at any evaluation time. Recovery scores were significantly better for butorphanol-treated than for control-group cats 10 minutes after extubation. Analgesia scores were significantly better for butorphanol-treated than for control-group cats between 5 and 24 hours after surgery. Fewer butorphanol-treated than control-group cats were lame at the time of discharge from the hospital. The first day after discharge, owners reported that percentages of butorphanol-treated cats that ate normally, acted normally, and had only mild or no lameness were significantly higher than percentages of control-group cats that did. Significant differences between groups were not detected the second day after discharge. CLINICAL IMPLICATIONS: Results suggest that for cats undergoing onychectomy, administration of butorphanol the day of surgery and the first full day after surgery provides effective analgesia and improves recovery, appetite, and gait.

Analgesia↗

PubMed1977

Double-blind placebo controlled oral analgesic comparison of butorphanol andpentazocine in patients with moderate to severe post-operative pain.

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 dose of butorphanol as well as pentazocine proved to be significantly (p less than 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 beeter 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 treatment 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 fo side-effects appeared low.

Adolescent↗

PubMed1993

Biopharmaceutical evaluation of transnasal, sublingual, and buccal disk dosage forms of butorphanol.

A series of three-way crossover randomized studies were conducted to evaluate the absolute bioavailability of butorphanol, a potent agonist-antagonist analgesic, from transnasal, sublingual, and buccal disk formulations in order to identify a practical alternative to oral administration. In each study, healthy male volunteers received 2 mg doses of butorphanol tartrate intravenously and either transnasally, sublingually or buccally. Serial blood samples were collected over 12 h and butorphanol plasma concentrations were determined by radioimmunoassay. The plasma concentration data were subjected to non-compartmental pharmacokinetic analysis. The elimination half-life of butorphanol was about 3-5 h and was independent of the route of administration. Absorption of butorphanol following transnasal administration was faster than that observed following sublingual or buccal administration. Mean absolute bioavailabilities of sublingual tablet and buccal disk formulation were only 19 per cent and 29 per cent, respectively, but for transnasal administration the value rose significantly, to 70 per cent. Based on the results of these studies, transnasal dosage form of butorphanol was selected for further clinical trials of treatment of moderate to severe pain.

Administration, Buccal↗

PubMed1986

Voluntary respiratory effects of butorphanol and fentanyl following barbiturate induction: a double-blind study.

Thirty-one healthy women undergoing outpatient gynecologic surgery were given either butorphanol or fentanyl following barbiturate induction, and various respiratory parameters were measured at intervals after administration of the study drugs. Both fentanyl and butorphanol caused comparable decrements in tidal volume and other respiratory parameters. However, seven of the 15 patients receiving fentanyl had significant respiratory depression that required assisted ventilation. One of the butorphanol patients experienced a 45-second self-limited respiratory depression. One of three butorphanol patients experiencing side effects required treatment for these effects, compared with seven of nine fentanyl patients who experienced adverse effects. It is concluded that butorphanol and fentanyl have comparable anesthetic effects, but butorphanol is safer in terms of respiratory and adverse effects.

Adolescent↗