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At least 19 recordsLinked to original sources
PubMed1986

Characterization of the effects of (+/-)-meptazinol, its individual enantiomers and N-methyl meptazinol on food consumption in the rat.

Both (+/-)-meptazinol (2 mg kg-1) and levorphanol (1 mg kg-1) produced hyperphagia over a 4 h period after intraperitoneal injection in free feeding rats during the daylight phase. The individual (+)- and (-)-enantiomers of meptazinol (2 mg kg-1 i.p.) induced comparable increases in cumulative food intake. N-methyl meptazinol (2-10 mg kg-1 i.p.), the quaternary analogue of meptazinol, produced no modification of food intake though it increased food consumption when injected intracerebroventricularly (10-100 micrograms per animal). Meptazinol and levorphanol hyperphagia was abolished by 1 mg kg-1 doses (i.p.) of the opioid antagonists naltrexone, naloxonazine and (-)-Mr 1452 but not by its (+)-enantiomer Mr 1453 which is not effective as an opioid antagonist. Intracerebroventricular administration of the delta-opioid antagonist ICI 154,129 (10 micrograms per animal) suppressed meptazinol but not levorphanol hyperphagia. It was concluded that meptazinol produces centrally mediated stereospecifically reversible hyperphagia through a mu-opioid receptor mechanism common to levorphanol, and also through delta-opioid receptor mechanism(s).

Animals↗
PubMed2006

Investigation of the binding mode of (-)-meptazinol and bis-meptazinol derivatives on acetylcholinesterase using a molecular docking method.

Molecular docking has been performed to investigate the binding mode of (-)-meptazinol (MEP) with acetylcholinesterase (AChE) and to screen bis-meptazinol (bis-MEP) derivatives for preferable synthetic candidates virtually. A reliable and practical docking method for investigation of AChE ligands was established by the comparison of two widely used docking programs, FlexX and GOLD. In our hands, we had more luck using GOLD than FlexX in reproducing the experimental poses of known ligands (RMSD<1.5 A). GOLD fitness values of known ligands were also in good agreement with their activities. In the present GOLD docking protocol, (-)-MEP seemed to bind with the enzyme catalytic site in an open-gate conformation through strong hydrophobic interactions and a hydrogen bond. Virtual screening of a potential candidate compound library suggested that the most promising 15 bis-MEP derivatives on the list were mainly derived from (-)-MEP with conformations of (S,S) and (SR,RS) and with a 2- to 7-carbon linkage. Although there are still no biological results to confirm the predictive power of this method, the current study could provide an alternate tool for structural optimization of (-)-MEP as new AChE inhibitors. [Figure: see text].

Acetylcholinesterase↗
PubMed1986

On the cholinergic component of action of meptazinol.

The effects of meptazinol, morphine and fentanyl on the indirect twitch contractions, the contractions produced by periarterial nerve stimulation, by field stimulation and by applied acetylcholine (ACh) were studied in rat isolated diaphragm and ileum respectively. Meptazinol (1-200 microM) increased the amplitudes of the indirect twitch tension in a dose-dependent manner. High concentrations of meptazinol (370 microM) reduced the twitch tension without the initial stimulation. The mean EC50 value of meptazinol-induced increase in twitch tension was 50 +/- 4.2 microM (n = 6). Morphine (2.9-290 microM) and fentanyl (2.9-290 microM) always reduced the amplitude of the twitch tension without initial stimulation. In the rat ileum, low concentrations of meptazinol (3.7-37 microM) increased the contractions produced by periarterial nerve stimulation, elicited at 10 or 20 Hz, in the presence of adrenergic blocking drugs, by 30%. Naloxone (1 microM) only partially reduced these contractions (by 25%), whereas atropine (1 microM) reduced these responses by 70%. Meptazinol (3.7 microM) increased the amplitude of the spontaneous contractions (by 50-100%) and sometimes this was accompanied by repetitive firing in the muscle. The twitch tension, in response to electrical field stimulation, was also increased by meptazinol (by 40-50%). At low concentrations, meptazinol produced no significant antagonism of applied ACh contracture, whereas at high concentrations, meptazinol (370 microM), morphine (29 microM) and fentanyl (29 microM) reduced the ACh response and shifted, to the right, the concentration-response curve, morphine being the most effective agent. Dose-ratios (test/control) of 100:4:2, with morphine, fentanyl and meptazinol, were obtained. Compared to meptazinol (relative potency = 1), morphine was 60 times as potent as meptazinol. Furthermore, the relative potency of meptazinol did not significantly change in the presence of naloxone, whereas those of morphine and fentanyl were changed significantly (by a factor of 10 and 2 respectively). These results showed that meptazinol, in low concentrations, may facilitate neuromuscular transmission, possibly via an increase in transmitter release. At high concentrations, meptazinol, like morphine and fentanyl, reduced the sensitivity of the post-junctional membrane to ACh. Furthermore, the blocking effect of meptazinol was only partially reduced by naloxone, and completely abolished by atropine in combination with naloxone. The latter effect may indicate a cholinergic mechanism in the action of meptazinol and that this may, in part, contribute to the analgesic effect of meptazinol.

Acetylcholine↗
PubMed1988

Protection against diisopropylfluorophosphate intoxication by meptazinol.

The protective action of meptazinol against diisopropylfluorophosphate (DFP) was evaluated in mice which were not receiving any other therapy and in preparations of electric eel AChE and horse serum BuChE. Meptazinol injected subcutaneously in mice produced a dose-dependent reduction in the mortality resulting from a LD99.1 (8 mg/kg sc) of DFP administered later. The effectiveness of protection was inversely correlated to the time between meptazinol and DFP administrations. Under these conditions, the ED50s (95% confidence limits) of meptazinol given 15, 30, and 60 min before poisoning were 7.2 (6.4-8.1), 15.8 (13.7-18.2), and 28 (23.5-33.3) mg/kg, respectively, while full protection (100% of survivors) was obtained with 15, 30, and 60 mg/kg drug doses, respectively. Meptazinol was completely ineffective against DFP-induced lethality when administered 3 min after the poison. The protective ratio of 30 mg/kg meptazinol injected 15 min before DFP was 5.0. Pretreatment of mice with 15, 30, and 60 mg/kg meptazinol 15 min before DFP (8 mg/kg) increased brain AChE activity in DFP-treated mice from 5 +/- 0.5% to 16.2 +/- 2.5%, 42.5 +/- 4%, and 81.2 +/- 4% of control values, respectively, while it failed to increase plasma BuChE activity. Finally, concentrations of meptazinol ranging between 0.1 and 10 microM were found to afford complete protection of eel AChE against irreversible inhibition by 40 microM DFP. By contrast, horse serum BuChE was not protected against the same inhibitor by concentrations of meptazinol up to 1 mM. It is concluded that protection against DFP intoxication by meptazinol is most probably due to its protective action toward AChE.

Acetylcholinesterase↗
PubMed1984

Meptazinol: a novel Mu-1 selective opioid analgesic.

Meptazinol is a unique centrally active opioid analgesic, differing in many respects from the classical opiates or mixed antagonists. Although the overall binding of a series of 3H-labeled opioids is displaced poorly (IC50 values greater than 55 nM), detailed competition studies show that meptazinol inhibits a portion of 3H-labeled opiate and opioid peptide binding quite potently, with IC50 value under 1 nM. Both additional competition studies and saturation studies indicate that the meptazinol-sensitive binding of the 3H-ligands corresponds to the high affinity, or mu-1, binding site. In other binding studies meptazinol has a sodium shift of 8.7, midway between that of morphine (22.5) and naloxone (1.6), suggesting that it is a partial agonist. Naloxonazine treatment 24 hr earlier attenuates meptazinol analgesia in both the mouse writhing and rat tail-flick assays. Spinal transection in the mouse completely eliminates the analgesic activity of high doses of meptazinol in the tail-flick assay, implying a supraspinal mechanism of action in that species. Given at equianalgesic doses, morphine (3.5 mg/kg i.v.) significantly lowers the pO2 over 20 mm Hg and raises the pCO2 over 10 mm Hg as measured in arterial blood samples, whereas meptazinol (10 mg/kg i.v.) has no significant effects on either. Equally important, meptazinol administered with morphine does not reverse the respiratory depressant actions seen with morphine alone, distinguishing meptazinol from other mixed agonist/antagonists. Thus, both the binding and in vivo pharmacological studies are consistent with a mu-1 selective mechanism for the opioid actions of meptazinol.

Analgesia↗
PubMed1984

Meptazinol cross-tolerance studies between morphine or oxotremorine.

The time course of the development of auto-tolerance to meptazinol as determined by combined heat and pressure nociceptive tests has been examined using two dose levels of meptazinol (10 mg and 30 mgkg-1s.c.) corresponding to the partial agonist and cholinergic components respectively. In mice treated twice daily with meptazinol for eight days, there was cross tolerance to morphine in both tests at each dose level of meptazinol. In chronic morphine treated mice challenged with meptazinol (30 mg kg-1 s.c.), there was no cross tolerance with morphine since meptazinol still retained its antinociceptive effects in both tests. Mice treated chronically with meptazinol (30 mgkg-1 s.c.) did not respond to the cholinomimetic agent oxotremorine, implying that there was cross tolerance between these two analgesics. These data suggest the existence of a one-way tolerance between morphine and meptazinol whilst at higher doses of meptazinol a full tolerance occurs with oxotremorine.

Animals↗
PubMed1985

Intramuscular meptazinol and morphine in postoperative pain.

Meptazinol is an agonist-antagonist opioid analgesic believed to be unique in its selectivity for mu1 (high affinity) receptors and its cholinergic activity. Our objectives were to determine the relative analgesic potency of intramuscular meptazinol and morphine and to compare mood and side effects in 102 patients with cancer who have postoperative pain. Meptazinol (50, 100, and 200 mg) and morphine (4, 8, and 16 mg) were given for moderate to severe pain in a double-blind, randomized but balanced, incomplete block design. Serial multiple assessments of pain, relief, mood, and side effects were made. The most precise estimates of relative analgesic potency indicate that meptazinol is equivalent to 10 mg morphine at 120 mg (95% confidence interval 80 to 170 mg) for peak effect and at 175 mg (95% confidence interval 125 to 270 mg) for total effect. Mean (+/- SE) times to peak effect and to remedication were 0.9 +/- 0.1 and 3.6 +/- 0.2 hours for meptazinol and 1.4 +/- 0.1 and 4.8 +/- 0.4 hours for morphine at equianalgesic peak effects. The percentages of subjects with one or more side effects were 18, 49, and 73 for graded meptazinol doses and 32, 49, and 65 for graded morphine doses. Mean numbers of side effects per subject were 0.3, 1.5, and 3.5 for meptazinol and 0.5, 0.7, and 1.7 for morphine. Profiles of side effects differed. Mood improvement and overall satisfaction were dose related and greater for morphine than for meptazinol. Side effects may limit the use of meptazinol in doses that relieve severe postoperative pain.

Adolescent↗
PubMed1987

Prevention of physostigmine-induced lethality by the opioid analgesic meptazinol in the mouse.

The prophylactic action of meptazinol against physostigmine- and neostigmine-induced lethality was evaluated in mice. Meptazinol proved to be effective against physostigmine (1 mg kg-1 i.p.), but not against neostigmine (0.5 mg kg-1 i.p.). The antagonism by meptazinol of physostigmine-induced poisoning was maximal when the drug was administered 15 min before physostigmine. Under these conditions the ED50 (95% confidence limits) of meptazinol was 24 (22.0-26.1) mg kg-1 s.c. A 30 mg kg-1 dose of the drug prevented lethality in 89% of the animals. The action of meptazinol was not antagonized by naloxone hydrochloride (2 mg kg-1 i.p.), injected 10 min before meptazinol. Pretreatment of mice with 30 mg kg-1 meptazinol 15 min before physostigmine (1 mg kg-1) poisoning increased brain acetylcholinesterase (AChE) activity on average, from 8 to 31% of control values. The protection of cholinesterases against physostigmine- and neostigmine-induced inactivation was demonstrated in vitro directly on purified preparations of the enzymes using a dilution method. The ED50 values (95% confidence limits) for the protective effect of meptazinol of electric eel AChE against 1 and 3 microM physostigmine and 1 microM neostigmine were 2.6 (1.4-4.9), 9.5 (5-18) and 3 (1.6-5.7) microM, respectively, while for protection of horse serum butyrylcholinesterase (BuChE) against the same inhibitors, the ED50 values were 12 (5.4-26.4), 42 (27-65.1) and 8 (3.6-17.6) microM, respectively. It is suggested that prevention of physostigmine-induced lethality by meptazinol is a consequence of its protective action on AChE in the central nervous system.

Acetylcholinesterase↗
PubMed2004

Antinociceptive effects of meptazinol and its isomers on carrageenan-induced thermal hyperalgesia in rats.

Using the latency of paw withdrawal (PWL) from a noxious thermal stimulus as a measure of hyperalgesia, the effects of i.p. injection of meptazinol and its isomers, 112824 and 112825, on carrageenan-induced thermal hyperalgesia were studied in awaked carrageenan-inflamed rats. Peripheral inflammation was induced by intraplantar (i.pl.) injection of carrageenan (2 mg/100 microl) into one hindpaw in rats. Carrageenan produced marked inflammation (edema and erythema) and thermal hyperalgesia in the injected paws, which peaked at 3 h after injection and showed little change in magnitude for another 3 h. Injection of 0.1 mg/kg meptazinol (i.p.) at 3 h after carrageenan had no effect on the PWLs of either inflamed or non-inflamed hindpaw during the next 100 min (P>0.05, n=8). At the dosage of 1 and 10 mg/kg, meptazinol produced marked anti-nociception and anti-hyperalgesia in non-inflamed and inflamed hindpaw, respectively (P<0.05, n=8-11). The prolonging effect of meptazinol on PWL in inflamed hindpaw was more potent than that in non-inflamed hindpaw. Pre-administration of 1.5 mg/kg naloxone significantly antagonized meptazinol-induced anti-nociception and anti-hyperalgesia. Intraperitoneal injection of an isomer of meptazinol, 112825 (1.5 mg/kg), but not 112824 (1 mg/kg), markedly increased the PWL of the non-inflamed hindpaw. Nevertheless, both the isomers produced similar anti-hyperalgesic effect to that of meptazinol (P<0.05, n=8), which was completely reversed by naloxone (1.5 mg/mg). The results suggest that meptazinol and its isomers have anti-nociceptive and anti-hyperalgesic properties with the former more potent. The effects are mainly mediated by mu opioid receptors. This study provides an important clue for extending clinical utilization of meptazinol and its isomers.

Analgesics, Opioid↗
PubMed1987

Human pharmacology and abuse potential of meptazinol.

Meptazinol was assessed in nine opioid abusers according to a double-blind, randomized, crossover design to determine if it produced typical morphine effects. A comparison of physiologic and subjective effects was made between morphine, 7.5, 15, and 30 mg, meptazinol, 70, 140, and 280 mg, and placebo. Both drugs constricted pupils. Meptazinol, 140 and 280 mg, decreased body temperature. Valid relative potency estimates of morphine to meptazinol were obtained for self-reported liking, opiate symptoms, and pupillary constriction. Meptazinol did not increase euphoria or sedation scale scores but did increase dysphoria scale scores. In the therapeutic dose range, meptazinol produced miosis, morphine-like identification and symptoms, limited liking, and some dysphoria. Dysphoria predominated at the 280 mg dose of meptazinol. From these data, it is concluded that meptazinol is not a typical morphine-like drug and has limited abuse potential.

Adult↗
PubMed1983

Preliminary clinical and pharmacokinetic experiences in the newborn when meptazinol is compared with pethidine as an obstetric analgesic.

Preliminary results on the disposition of meptazinol in the neonate are reviewed. Meptazinol has a half-life of 3.4 hours compared with 22.7 hours for pethidine. In a randomised double blind trial of 100 patients the depressant effects in the newborn of meptazinol and pethidine were compared. There was no difference in the Apgar scores at 1 and 3 minutes. Weight loss and the incidence of neonatal jaundice were less when mothers received meptazinol although these differences did not reach statistical significance. However, the number of infants considered fit for discharge by the 6th day was significantly greater in the meptazinol groups. In 43 cases transcutaneous monitoring of arterial PO2 was carried out for 30 minutes following delivery. Although the mean PaO2 was similar for meptazinol and pethidine, significant variations in the PaO2 of 2.0 kPa or greater and significant neonatal activity as judged by episodes of crying and movement, were recorded in the meptazinol group. The results of the trial suggest that meptazinol may have less depressant effects on the newborn, and may be preferable to pethidine as an obstetric analgesic.

Anesthesia, Obstetrical↗
PubMed1989

Meptazinol and morphine in postoperative pain assessed with a new method for onset and duration.

Meptazinol, m-(3-ethyl-1-methyl-hexahydro-1-H-azepin-3-yl) phenol hydrochloride is a centrally active opioid analgesic with a specificity for the mu-1 receptor. It has been reported to lack many of the side effects commonly observed with morphine and morphinelike drugs in man. The objective of this study was to assess the analgesic efficacy and safety of meptazinol (50 mg and 100 mg) relative to morphine (5 mg and 10 mg) when administered intramuscularly for the treatment of postoperative pain. In addition, a new clinical method for measuring onset and duration and a statistical technique for evaluating the study data are presented. One hundred and seventeen patients were evaluated for 6 hours in a randomized double blind, single dose, parallel-groups trial. Estimates of relative potency for hourly pain and relief parameters, and the summary variables sum of pain intensity differences (SPID) and total pain relief (TOTPAR) were performed. The estimate of relative potency of meptazinol to morphine for pain relief was 0.19 at 1/2 hour (i.e. 100 mg of meptazinol was approximately equivalent to 20 mg of morphine). Thereafter, there was a rapid decline of efficacy for meptazinol, with a relative potency estimate of 0.12 at 1 hour and 0.06 at 2 hours. The distribution functions for several time related events were estimated including time to onset, duration and time to remedication. The two drugs had approximately equal onset, but meptazinol had significantly shorter duration. More patients on meptazinol required remedication with a rescue analgesic and at an earlier time than patients on morphine.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1980

A double-blind comparison of meptazinol with pethidine in postoperative pain.

Three groups each of 24 patients who had undergone total abdominal hysterectomy were studied on the 1st day after operation. Under double-blind conditions, group 1 compared meptazinol 60 mg with pethidine 100 mg, group 2, meptazinol 75 mg with pethidine 100 mg and group 3, meptazinol 100 mg with pethidine 100 mg. The drugs were given i.m. Analgesic activity was assessed by patients rating their pain before and 1 h after the administration of each treatment and by patient and investigator preference for treatment. From the pain relief score, pethidine was not significantly better than any dose of meptazinol in relieving pain. Patients preferred pethidine 100 mg to meptazinol 60 mg (P less than 0.01, McNemar's test), but there was no significant difference between meptazinol and pethidine for observer or patient preference when the dose of meptazinol was increased to 75 mg or 100 mg.

Adult↗
PubMed1983

Effects of graded oral doses of meptazinol and pentazocine in comparison with placebo on experimentally induced pain in healthy humans.

The opioid agonist/antagonist meptazinol has proven to exert significant analgesia in a series of painful conditions. This study investigated the effects of single oral doses of meptazinol 100, 200, and 400 mg in comparison with pentazocine 50 and 100 mg and with placebo on experimentally induced pain. In addition, the side effect profiles were assessed. Twenty-four healthy subjects participated each in six experiments in which they received, in random double-blind fashion, each of the treatments. Every experiment comprised 10 series of measurements, two before and eight after drug administration, carried out at 30 min intervals. Meptazinol produced significant dose-related increases of threshold and tolerance to electrically and thermally induced pain. Meptazinol 400 mg was significantly superior to placebo in all pain measures and proved as effective as pentazocine 50 and 100 mg, which yielded about equal effects. Meptazinol 200 mg was significantly weaker than pentazocine 50 mg and differed significantly from placebo only in its effects on pain tolerance. Meptazinol did not cause any severe side effects or systematic alterations of respiration, blood pressure, heart rate and central nervous functions. Pentazocine caused a higher number and more severe side effects, one subject reporting severe dysphoria after pentazocine 100 mg. The results give further evidence that meptazinol is well suited to replace other opioid analgesics compromised by a high incidence of adverse effects.

Adult↗
PubMed1983

Antiarrhythmic actions of meptazinol, a partial agonist at opiate receptors, in acute myocardial ischaemia.

1 The intravenous administration, to anaesthetized rats, of meptazinol (1 and 2 mg kg-1), a partial agonist at opiate receptors, greatly reduced the incidence of ventricular extrasystoles that resulted from acute coronary artery occlusion. The incidence of ventricular fibrillation (VF) was reduced from 50% (in the controls) to 10% and the mortality from 30% to zero. 2 In similar doses, pretreatment with meptazinol also reduced ventricular arrhythmias, including fibrillation, in conscious rats subjected to coronary artery occlusion. In this model, survival at 16 h was increased from 27% in the controls to 50% and 83% respectively in rats pretreated with 1 and 2 mg kg-1 of the drug. 3 In antiarrhythmic doses, meptazinol had little effect on either heart rate or systemic arterial blood pressure. 4 Intracellular action potential recordings from papillary muscle removed from rats given meptazinol (2 mg kg-1) 15 min previously showed an increase in APD50 and APD90 of more than 40%. There was no effect on dV/dtmax. When superfused with meptazinol in vitro normal rat papillary muscle stimulated at 1 or 3 Hz showed an increase in APD90 and a decrease in dV/dtmax. 5 The antiarrhythmic effect of meptazinol in these models can probably be explained by direct actions on the cardiac muscle action potential (increase in APD) although effects on opiate receptors cannot be ruled out. It is suggested that meptazinol might be useful in relieving pain, and in reducing the severity of arrhythmias in the early stages of acute myocardial infarction.

Action Potentials↗
PubMed1985

Comparison of the cardiovascular effects of meptazinol and naloxone following haemorrhagic shock in rats and cats.

The cardiovascular effects of the opioid mixed agonist-antagonist, meptazinol, and the opioid antagonist, naloxone, have been evaluated in conscious rats, anaesthetized rats and anaesthetized cats following the induction of haemorrhagic shock. The mean arterial pressure of conscious rats decreased by 17-29 mmHg following a haemorrhage of 20% of blood volume. Meptazinol (17 mg kg-1, i.m.) administered after haemorrhage evoked a rapid and sustained increase in mean arterial pressure to pre-haemorrhage levels. Naloxone (10 mg kg-1, i.v.) also increased mean arterial pressure to a level significantly higher than post-haemorrhage values. Neither haemorrhage nor subsequent drug treatments evoked significant changes in the heart rates of conscious rats. In anaesthetized rats, 20% haemorrhage evoked decreases in mean arterial pressure, heart rate and cardiac output. Blood flow to the heart, skin, skeletal muscle, kidneys, spleen and liver (arterial) was decreased. Meptazinol and naloxone increased blood pressure and total peripheral resistance, but did not significantly alter heart rate or cardiac output. Hepatic arterial flow decreased further in both drug and vehicle treated groups. In addition meptazinol slightly reduced skeletal muscle flow. In anaesthetized cats 40% haemorrhage decreased mean arterial pressure by 46 +/- 3 mmHg. An intravenous infusion of either meptazinol or naloxone (cumulative 2 mg kg-1, i.v.) partially restored blood pressure. In experimental animal models of haemorrhagic shock, meptazinol has a similar cardiovascular profile to naloxone. The established analgesic activity of meptazinol may confer an advantage in some shock states.

Anesthesia↗
PubMed1986

Meptazinol has a similar agonist action on opioid receptors in field-stimulated mouse vas deferens and guinea-pig ileum.

The effects of the opioid receptor agonist RX783006 and of the opioid receptor partial agonist (+)-meptazinol have been examined on electrically induced twitch responses of the guinea-pig isolated ileum and of the mouse isolated vas deferens. Log10 concentration-tissue state curves were determined for (+)-meptazinol and RX783006, alone, in combination and in the presence of naloxone (30 nM). Analysis of these log10 concentration-tissue state curves using the null equations derived and tested in the preceding paper indicates that the opioid agonist action of (+)-meptazinol on mouse vas deferens is quantitatively similar to that on guinea-pig ileum. The results also suggest that (+)-meptazinol acts as a functional antagonist on the guinea-pig ileum as well as on the mouse vas deferens. The potency of (+)-meptazinol relative to RX783006 has been measured by an indirect method which should eliminate any functional antagonistic action of (+)-meptazinol. This method gives a relative potency of (+)-meptazinol in both tissues which is three to six times greater than that measured directly on guinea-pig ileum. This discrepancy may be due to experimental error but it may also indicate that direct measurements on guinea-pig ileum underestimate the agonist potency of this compound on opioid receptors.

Animals↗