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PubMed2005

Butorphanol dependence increases hippocampal kappa-opioid receptor gene expression.

Butorphanol is a synthetic opioid agonist/antagonist analgesic agent, which exerts its effects mainly via kappa-opioid receptors. Characterizations of the gene expression levels of the mRNA for and protein levels of the kappa-opioid receptor in different brain regions of rats are essential for investigating possible mechanisms in the development of physical dependence on and withdrawal from butorphanol. Animals were rendered dependent by intracerebroventricular (i.c.v.) infusion of butorphanol (26 nmol/microl/hr) via osmotic minipumps for 3 days. Rats were sacrificed immediately (dependent group) or 7 hr after discontinuation of i.c.v. butorphanol infusion (withdrawal group). Expression levels of the mRNA for the kappa-opioid receptor, as detected by reverse transcription-polymerase chain reaction followed by Southern blot analysis, were significantly increased in the cerebral cortex, striatum, and midbrain, including thalamus, hippocampus, and pons, in animals dependent on butorphanol. In both dependent and withdrawal groups, Western blot analysis of kappa-opioid receptor protein levels showed significant increases in the amygdaloid nucleus, paraventricular thalamus, and thalamus. However, in the withdrawal group, there were significant decreases in the hippocampus and cortical regions, including the frontal, parietal, and temporal cortex. Regional changes in the mRNA for and protein levels of the kappa-opioid receptor focus attention on highly special roles for this receptor in the development of physical dependence on and the expression of withdrawal from butorphanol dependence.

Animals↗

PubMed1994

The effects of age and sex on the systemic availability and pharmacokinetics of transnasal butorphanol.

We have studied the effects of age and sex on the pharmacokinetics and the systemic availability of transnasal butorphanol in a randomized, two-way, cross-over study of 48 subjects: young men and women, and elderly men and women. Each subject took a single 1 mg dose of intravenous and transnasal butorphanol tartrate on separate occasions with a one-week washout period. Blood samples were collected over 16 hours. Plasma butorphanol concentrations were determined using radioimmunoassay. The AUC of plasma butorphanol concentrations after an intravenous injection were higher in the elderly women than in the other groups. However, there were no significant differences in Cmax and AUC between the groups after transnasal administration. The mean systemic availability of transnasal butorphanol was about 70%, except for the elderly women (48%). After intravenous and transnasal administration, the half-life and mean residence time were greater in the elderly than the young. Clearance was lower in women than men. Apparent volume of distribution was higher for elderly men than the others. The age- and sex-related changes in the pharmacokinetics of transnasal butorphanol are not large enough to necessitate dosage differences.

Administration, Intranasal↗

PubMed1995

Simultaneous measurement of biogenic amines and their metabolites in rat brain regions after acute administration of and abrupt withdrawal from butorphanol or morphine.

Changes in levels of biogenic amines and metabolites were measured using high performance liquid chromatography fitted with an electrochemical detection in various rat brain regions after acute administration of and abrupt withdrawal from continuous intracerebroventricular infusion of butorphanol (a mu/delta/kappa mixed opioid receptor agonist) or morphine (a mu-opioid receptor agonist). A single dose of butorphanol (26 nmol/5 microliters) or morphine (26 nmol/5 microliters) increased levels of 3,4-dihydroxyphenylacetic acid in the striatum and limbic region and of homovanilic acid in the cortex, striatum, and limbic region. In animals which had been infused with butorphanol (26 nmol/microliters/hr) or morphine (26 nmol/microliters/hr) for 3 days, an increase in dopamine turnover was observed. The levels of 3,4-dihydroxyphenylacetic acid was decreased and that of homovanilic acid was increased in the striatum, limbic region, and midbrain immediately after termination of opioid infusion. Both dopamine metabolites (in these areas) were decreased at 2 and 6 hr after butorphanol or morphine withdrawal. Changes in norepinephrine, serotonin, and 5-hydroxyindoleacetic acid levels in some brain regions were observed in the morphine-, but not in butorphanol-dependent rats. These data suggest that the increase and the decrease in dopaminergic activity, but not noradrenergic and serotonergic neurons, in the some brain regions are closely associated with the production of antinociception of and the expression of withdrawal syndrome from butorphanol and morphine, respectively.

Animals↗

PubMed2005

Oral midazolam and oral butorphanol premedication.

OBJECTIVE: To evaluate the efficacy of oral midazolam and oral butorphanol for their sedative analgesic effects in children. METHODS: Sixty children, aged 2 to 10 yrs, of ASA physical status I and II, scheduled for surgical procedures of 1 to 2 hrs duration were randomized to one of the two groups. Group I: children received midazolam 0.5 mg/kg orally and Group II: children received butorphanol 0.2 mg/kg orally. Score of the children was assessed every 5 minutes till the induction of anesthesia. Intraoperative and postoperative analgesic requirement was recorded along with postoperative recovery and complications. RESULTS: The groups were identical regarding the patient's characteristics, hemodynamic variables, duration of surgery and awakening time. Less time was required for the onset and time of maximum sedation in the butorphanol group (p<0.05). Sedation scores were similar among the groups at all time intervals, while the scores were higher in the butorphanol group at the time of induction (p<0.05). Less number of children required intraoperative and postoperative rescue analgesia in the butorphanol group (p<0.05). Statistically significant difference was found among the groups in respect to complete amnesia (50% in group I vs 80% I group II, p<0.05) and recollection (40% in group I vs 10% in group II, p<0.05). CONCLUSION: Oral butorphanol is comparable to oral midazolam in children but analgesia along with sedation is an additional advantage which makes it better than midazolam without a significant increase in side effects.

Administration, Oral↗

PubMed1978

A double-blind comparison of butorphanol and meperidine in labour: maternal pain relief and effect on the newborn.

Butorphanol tartrate 1 mg and 2 mg were compared in 80 normal mothers at term in a double-blind study with meperidine hydrochloride 40 mg and 80 mg for the relief of pain in labour. Butorphanol was found to be as effective as meperidine in relieving pain in labour. The foetal condition, as measured by ECG monitoring, Apgar scores, time to sustained respiration, umbilical venous H+ (pH) and PCO2, and a general nursery survey were comparable for meperidine and butorphanol. No psychomimetic phenomena were seen. Assays indicated that both butorphanol and meperidine crossed the placenta. The mean concentration of butorphanol in neonatal serum was 0.84 times maternal serum at 1.5 to 3.5 hours after intramuscular administration of a single or two successive doses of butorphanol 1 mg or 2 mg to the mother. The mean concentrations for meperidine in neonatal serum was 0.89 times maternal serum at 0.85 to 3.6 hours after intramuscular administration of meperidine 40 mg or 80 mg to the mother. Neither analgesic caused severe depression of the infant except for one meperidine-treated case.

Anesthesia, Obstetrical↗

PubMed1993

Involvement of delta-opioid receptors in physical dependence on butorphanol.

Butorphanol, a synthetic agonist/antagonist, has been shown to act on mu-, delta- and kappa-opioid receptors. However, the relative involvement of opioid receptor subtypes in mediating butorphanol dependence is not known. In the present study, naltrindole, a delta-selective non-peptide antagonist, was administered intracerebroventricularly (i.c.v.) to mask supraspinal delta-opioid receptors before and during the induction of butorphanol dependence. Treatment with naltrindole (0.1, 1, or 10 nmol/5 microliters per rat) significantly blocked naloxone-, a nonspecific antagonist, precipitated butorphanol withdrawal behaviors (escape behavior, teeth-chattering, wet shakes, forepaw tremors, ptosis, diarrhea, body weight loss, and hypothermia) at all doses tested, and decreased ejaculation at 0.1 nmol in butorphanol-infused rats. In contrast, naltrindole treatment had no effect on yawning, nor urination. These results indicate that central delta-opioid receptors are involved in mediating butorphanol dependence in rats.

Animals↗

PubMed1996

Profiling impurities and degradants of butorphanol tartrate using liquid chromatography/mass spectrometry and liquid chromatography/tandem mass spectrometry substructural techniques.

A rapid and systemic strategy based on liquid chromatography/mass spectrometry (LC/MS) profiling and liquid chromatography/tandem mass spectrometry (LC/MS/MS) substructural techniques was utilized to elucidate the degradation products of butorphanol, the active ingredient in stadol NS. This strategy integrates, in a single instrumental approach, analytical HPLC, UV detection, full-scan electrospray mass spectrometry, and tandem mass spectrometry to rapidly and accurately elucidate structures of impurities and degradants. In these studies, several low-level degradation products were observed in long-term storage stability samples of bulk butorphanol. The resulting analytical profile includes information on five degradants including molecular structures, chromatographic behavior, molecular weight, UV data, and MS/MS substructural information. The degradation products formed during long-term storage of butorphanol tartrate included oxidative products proposed as 9-hydroxy-and 9-keto-butorphanol, norbutorphanol, a ring-contraction degradant, and delta 1, 10 a-butorphanol. These methodologies are applicable at any stage of the drug product cycle from discovery through to development. This library of butorphanol degradants provides a foundation for future development work regarding product monitoring, as well as a useful diagnostic tool for new degradation products.

Administration, Inhalation↗

PubMed1979

Butorphanol and meperidine compared in patients with acute ureteral colic.

Pain relief was evaluated in 81 patients with acute ureteral colic and the confirmed presence of a calculus. A randomized double-blind comparison of intramuscular 2 and 4 mg. butorphanol and 80 mg. meperidine was used. Pain intensity and pain relief were evaluated at half hour and hourly intervals for 4 hours. A 2 mg. dose of butorphanol was found to be analgesically equivalent to 80 mg. meperidine, while a 4 mg. dose of butorphanol was found to be more effective than 80 mg. meperidine and 2 mg. butorphanol. Each patient received up to 2 doses of analgesic medication when necessary. There was no significant difference in the incidence of side effects among treatments. One patient had visual hallucinations after a 2 mg. dose of butorphanol, possibly owing to its antagonistic activity to significant narcotic experience given previously at another hospital. There was no other evidence of toxicity with butorphanol. It was found to be a safe, effective and wall tolerated drug for the treatment of ureteral colic and is recommended in place of narcotics.

Acute Disease↗

PubMedDate not supplied

Changes in plasma cortisol concentrations in bitches in response to different combinations of halothane and butorphanol, with or without ovariohysterectomy.

Changes in plasma cortisol concentrations were assessed in bitches in response to nine treatments: control, anaesthesia, analgesia, analgesia followed by anaesthesia, anaesthesia followed by analgesia at intubation, anaesthesia followed by analgesia at extubation, anaesthesia plus surgery, analgesia followed by anaesthesia plus surgery, and anaesthesia plus surgery followed by analgesia. The anaesthetic was halothane, the analgesic was butorphanol (0.4 mg kg(-1)) and the surgery was ovariohysterectomy. Blood samples, for plasma cortisol assays, were taken regularly from before treatment for five hours and then again after 24 hours. A small transient rise in plasma cortisol concentration in the control group was attributed to mild distress associated with novel experiences. A more pronounced and protracted rise in cortisol concentration in the analgesia group was ascribed to a dysphoric state of bitches under the influence of the agonist-antagonist butorphanol. Halothane anaesthesia alone resulted in no change in plasma cortisol concentration. When butorphanol was given after anaesthesia was induced or while the animal was still under the influence of anaesthesia (immediately after tracheal extubation), there was no immediate rise in plasma cortisol concentration and low concentrations were maintained for up to 60 minutes after halothane withdrawal. A marked rise in plasma cortisol concentration, which was sustained above pretreatment values for at least five hours, occurred in all surgery groups. Giving intravenous butorphanol 30 minutes prior to surgery had no effect on the surgically-induced rise in plasma cortisol concentration and no effect on the postsurgical plasma cortisol concentration. In contrast, butorphanol given at extubation did reduce plasma cortisol concentrations during the postsurgical period. These observations did not support the hypothesis that preoperative use of butorphanol would reduce the cortisol response after surgery under halothane anaesthesia.

Analgesia↗

PubMed2003

Agonist/antagonist properties of nalbuphine, butorphanol and (-)-pentazocine in male vs. female rats.

To determine whether sex differences in the effects of mixed-action opioids could be due to differential activity at mu or kappa receptors, agonist/antagonist properties of nalbuphine, butorphanol and (-)-pentazocine were compared in male vs. female rats using a diuresis test. In water-loaded rats (2-h test), nalbuphine and (-)-pentazocine dose-dependently increased urination similarly in both sexes, whereas butorphanol increased urination more in females than in males on a ml/kg basis. The diuretic effects of all three opioids were at least partially blocked by the kappa receptor-selective antagonist nor-binaltorphimine (nor-BNI, 5 mg/kg) in both sexes. Kappa receptor-mediated antagonism of diuresis induced by U69,593 (0.56 mg/kg) was only observed with butorphanol in males. In water-loaded rats (1-h test), nalbuphine did not suppress, and butorphanol and (-)-pentazocine significantly suppressed urination in males only; all three mixed-action opioids dose-dependently blocked the antidiuretic effect of the selective mu agonist fentanyl (0.056 mg/kg) in both sexes. The ability of nalbuphine and (-)-pentazocine to block fentanyl-induced antidiuresis was not affected by pretreatment with nor-BNI in either sex. In contrast, the ability of butorphanol to block fentanyl-induced antidiuresis was attenuated by pretreatment with nor-BNI in males but not in females. These results suggest that sex differences in the effects of these mixed-action opioids are primarily due to their greater relative efficacy at the mu receptor in male than in female rats; butorphanol also may have greater efficacy at kappa receptors in females than in males.

Animals↗

PubMed1988

Comparison of intramuscular analgesic activity of butorphanol and morphine in patients with sickle cell disease.

This double-blind study compared the analgesic effects of morphine with those of butorphanol in patients who presented with pain because of sickle cell crisis. Patients were placed at bed rest, administered IV hydration, and randomly assigned on each visit to receive either 2 mg IM butorphanol or 6 mg IM morphine every 30 to 60 minutes as needed to produce a pain intensity of 50 mm or less on the linear analog pain scale until the patient was discharged. Linear analog scale for pain and pain relief, level of alertness, and vital signs were assessed at 60 and 120 minutes after each study drug dose, before additional doses, and at discharge. Eighteen patients (12 men, six women; mean age, 29.3 +/- 7.7 years) were studied. Six received only morphine, six received only butorphanol, and six received each treatment at some time during the study period, resulting in 45 randomizations to treatment. The two therapies did not differ significantly (P greater than .40) with respect to pain or relief of pain scores, level of alertness, or vital signs. The discharge rate was 69.6% and 68.2% with morphine and butorphanol, respectively (P = .92). The incidence of adverse effects was 13% and 23% with morphine and butorphanol, respectively (P = .46). We conclude that morphine and butorphanol are equally effective in the treatment of sickle cell crisis pain.

Adolescent↗

PubMed2000

kappa-opioid agonist stimulated regional distribution of [(35)S]GTPgammas binding in butorphanol continuously infused rat.

Butorphanol is a mixed agonist/antagonist opioid analgesic agent, which exerts its effects mainly by interaction with the kappa-opioid receptor. Opioid receptors are coupled to G proteins of G(i)/G(o) family, and recently a decrease in micro-opioid activation of G proteins has been reported in specific brainstem nuclei after chronic morphine administration. The influence of centrally administered butorphanol on agonist-stimulated G protein coupling was examined in the rat brain, using in situ guanylyl-5'-O-(gamma-[(35)S]thio)-triphosphate (GTPgammaS) binding autoradiography. Rats were treated with butorphanol (26 nmol/microl/h) by intracerebroventricular infusion via osmotic minipumps for 3 days. The distribution of [(35)S]GTPgammaS binding in the brain 7 h after the termination of butorphanol infusion was measured in the presence or absence of the selective kappa-opioid agonist, U-50,488. This agonist significantly increased [(35)S]GTPgammaS binding in the parietal cortex, caudate putamen, thalamus, and central gray of control rats, but not in those regions of the butorphanol-infused animals. These results suggest that chronic administration of butorphanol developed tolerance and abolished U-50,488 activation of G proteins in these brain areas.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

PubMed2004

Pharmacokinetics of butorphanol tartrate administered from single-dose intranasal sprayer.

PURPOSE: The pharmacokinetics and tolerability of single and multiple doses of intranasal butorphanol tartrate using a single-dose metered sprayer were studied. METHODS: In this randomized, open-label, two-way crossover study, 24 healthy subjects received either 1 or 2 mg of intranasal butorphanol as a single dose (treatment A) and 1 or 2 mg of intranasal butorphanol every six hours for seven doses (treatment B). During phase 1, 12 subjects selected at random received a single 1-mg dose and the other 12 a single 2-mg dose. During phase 2, those who received the 1-mg single dose received 1 mg every six hours for seven doses. During phase 3, those who received the 2-mg single dose received 2 mg every six hours for seven doses. Serial blood samples were collected over 12 hours. Pharmacokinetic parameters were determined using noncompartmental methods. RESULTS: Mean (coefficient of variation) values for the area under the concentration-versus-time curve (AUC) from time zero to infinity (AUC0-infinity) were 4.15 (26.4%) and 10.42 (19.6%) ng.hr/ml after single doses of 1 and 2 mg of butorphanol, respectively. At steadly state, mean values for the AUC from time zero to the dosing interval (AUC0-tau) were 4.82 (40.2%) and 10.60 (22.3%) ng.hr/mL, respectively. The accumulation indices were around 2 for both the 1- and 2-mg doses. Median time to maximum concentration values ranged from 15 to 30 minutes for each treatment. Dose-normalized parameters AUC0-infinity. AUC0-tau and maximum concentration (Cmax) were significantly larger after a single 2-mg versus 1-mg dose (p < 0.05). CONCLUSION: Intranasal butorphanol has rapid absorption and predictable accumulation after multiple doses administered with single-dose metered sprayers. Intranasal administration of butorphanol was well tolerated and adverse events were generally mild to moderate in severity and as expected for this drug.

Administration, Intranasal↗

PubMed1996

Pharmacokinetics of epidural butorphanol in isoflurane-anaesthetized dogs.

Sixteen healthy male dogs were used at random in this protocol. The dogs were anaesthetized with isoflurane in oxygen. Eight of the dogs received 0.25 mg/kg of butorphanol (group B) and the others an equal volume of isotonic saline (group S) administered by a catheter inserted in the lumbosacral epidural space. Butorphanol concentrations in plasma and cerebrospinal fluid (CSF) were measured using high-performance liquid chromatography with electrochemical detection. Maximum concentration of butorphanol and time to obtain this concentration were 42.28 ng/mL at 13.88 min in blood, and 18.03 ng/mL at 30 min in CSF. Volume of distribution, clearance, mean distribution and elimination half-lives were respectively 4.39 L/kg, 2.02 L/h.kg, 16.5 min and 189.1 min. Mean isoflurane minimal alveolar concentration values for group B obtained following hind- or forelimb stimulation decreased by 31% after epidural butorphanol. Cutaneous analgesia (to pin-prick test) persisted for 3 h after the end of isoflurane anaesthesia in group B and was in correlation with the plasmatic analgesic dose of butorphanol (9 ng/mL). These results suggested that analgesia was predominantly obtained by action of butorphanol on the supraspinal structures following its vascular systemic absorption.

Analgesia, Epidural↗

PubMed1991

Transnasal butorphanol: a new method for pain relief in post-cesarean section pain.

This study was undertaken to evaluate the efficacy and the safety of transnasal butorphanol (TNB) compared to intravenous butorphanol (IVB) in 186 patients experiencing moderate to severe post-cesarean section pain. Patients were randomly assigned to five groups in a double-blind fashion: Group I (n = 37) received 2 mg IVB, Group II (n = 38) 2 mg TNB, Group III (n = 36) 1 mg TNB followed by a repeat dose of 1 mg TNB at 60 min, Group IV (n = 38) 0.5 mg TNB followed by a repeat dose of 0.5 mg at 60 min, and Group V (n = 37) received placebo. All administrations were double dummy. Pain intensity and relief were noted and the incidence of side effects was recorded. Remedication with the same study drug was allowed up to 72 h. Onset of analgesia was more rapid in the 2 mg IV group compared to the three TN groups: 5 min vs 15 min, respectively. However, the 2 mg and the 1-1 mg TN groups had a longer duration of analgesia, approximately 4.5 h, compared to 3.0 h for the 2 mg IV group (P less than 0.05). Somnolence was dose related and was the most frequent side effect, and was less frequent when the TN dose was divided into 2 doses administered 1 h apart. Multiple doses of TNB and IVB were safe and clinically acceptable up to 3 days at all doses studied. There were no incidences of nasal mucosa irritation, or cardiovascular or respiratory depression. It is concluded that transnasal butorphanol represents a safe and effective alternative to injectable butorphanol for post-cesarean section pain and offers a better and longer duration of analgesia compared to IV butorphanol. The optimum dose seems to be 2 mg TN butorphanol and it is tolerated better when divided into 1 mg increments, given 1 h apart.

Administration, Intranasal↗

PubMed1994

Epidural butorphanol does not reduce side effects from epidural morphine after cesarean birth.

In this prospective, double-blind, randomized study of women undergoing elective cesarean birth, the hypothesis that epidural butorphanol in various doses could effectively reduce or eliminate the side effects caused by epidural morphine was tested. Patients were randomly assigned to one of four groups. All received a standard epidural anesthetic and 20 min after delivery each received 3 mg epidural morphine with either 1 mg butorphanol (Group A), 2 mg butorphanol (Group B), 3 mg butorphanol (Group C), or 3 mL normal saline (Group D). Patient evaluations were made preoperatively and 2, 8, and 24 h after delivery. These consisted of visual analog scores for pain, satisfaction, nausea, itch, and somnolence. At each evaluation, a CO2 challenge test, using portable equipment, was performed. Data from 71 patients were analyzed and all four groups were comparable in terms of age, height, weight, level of sensory block, and volume of local anesthetic used. There were no significant differences among groups in terms of pain, satisfaction, nausea, or pruritus. Groups A, B, and C had significantly higher somnolence scores at 8 h compared to Group D (P < 0.001). There were no significant differences among groups in CO2 challenge test data at any point during the study, but overall a reduced sensitivity to CO2 after opioid administration was observed across all groups. There were no clinically significant incidents of respiratory depression. Epidural butorphanol, in doses of 1-3 mg, failed to reduce the side effects from 3 mg epidural morphine given after cesarean birth. Patients who received epidural butorphanol reported significantly higher levels of somnolence.

Anesthesia, Epidural↗

PubMed2005

Butorphanol: effects of a prototypical agonist-antagonist analgesic on kappa-opioid receptors.

The opioid analgesic, butorphanol (17-cyclobutylmethyl-3,14-dihydroxymorphinan) tartrate is a prototypical agonist-antagonist opioid analgesic agent whose potential for abuse has been the cause of litigation in the United States. With a published affinity for opioid receptors in vitro of 1:4:25 (mu:delta:kappa), the relative contribution of actions at each of these receptors to the in vivo actions of the drug are an issue of active investigation. A body of evidence has been developed which indicates that a substantial selective action of butorphanol on the kappa-opioid receptor mediates the development of tolerance to butorphanol and cross-tolerance to other opioid agonists; to the production of dependence upon butorphanol, particularly in the rodent; and to compensatory alterations in brain opioid receptor-effector systems. This perspective will identify the current state of understanding of the effects produced by butorphanol on brain opioid receptors, particularly on the kappa-opioid receptor subtype, and on the expression of phosphotyrosyl proteins following chronic treatment with butorphanol.

Analgesics, Opioid↗

PubMed2006

Electroencephalographic and electromyographic changes during the use of detomidine and detomidine-butorphanol combination in standing horses.

Clinically, the use of detomidine and butorphanol is suitable for sedation and deepening of analgosedation. The aim of our study was to establish the influence of detomidine used alone and a butorphanol-detomidine combination on brain activity and to evaluate and compare brain responses (using electroencephalography, EEG) by recording SEF90 (spectral edge frequency 90%), individual brain wave fractions (beta, alpha, theta and delta) and electromyographic (EMG) changes in the left temporal muscle in standing horses. Ten clinically healthy cold-blooded horses were divided into two groups of five animals each. Group I received detomidine and Group II received detomidine followed by butorphanol 10 min later. SEF90, individual brain wave fractions and EMG were recorded with a pEEG (processed EEG) monitor using computerised processed electroencephalography and electromyography. The present study found that detomidine alone and the detomidine-butorphanol combination significantly reduced SEF90 and EMG, and they caused changes in individual brain wave fractions during sedation and particularly during analgosedation. The EMG results showed that the detomidine-butorphanol combination provided greater and longer muscle relaxation. Our EEG and EMG results confirmed that the detomidine-butorphanol combination is safer and more appropriate for painless and non-painless procedures on standing horses compared to detomidine alone.

Analgesics, Opioid↗