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Simultaneous determination of codeine and morphine in biological samples by gas chromatography with electron capture detection.

A sensitive gas chromatographic method for the simultaneous determination of codeine and morphine in plasma and brain samples is described. The method involves solvent extraction of the compounds from plasma, derivatization with pentafluoropropionic anhydride and subsequent separation on a 3% OV-17 column. The quantification is performed with electron capture detection. The sensitivity of the method (0.75 ng of morphine and 7.5 ng of codeine in a sample) makes it especially useful for pharmacokinetic investigations. The method was successfully applied to determine the time course of codeine and its metabolite morphine after intravenous administration of codeine to the rat.

Animals↗

Blood-brain barrier: penetration of morphine, codeine, heroin, and methadone after carotid injection.

Labeled morphine, codeine, heroin, or methadone was injected as a bolus into the common carotid artery of the rat, and the rat was decapitated 15 seconds later. The brain uptake of the drug was calculated by measurement of the brain content of the drug as a percentage of a labeled, highly diffusible reference substance simultaneously injected. The uptake of morphine was below measurability; the uptake of codeine was 24 percent; heroin, 68 percent; and methadone, 42 percent. Brain uptakes of morphine and codeine were also studied after intravenous injection and correlated well with uptakes after carotid injection; the uptake of codeine being nearly complete by 30 seconds. These studies indicate that brain uptake of certain of these drugs is very rapid and that uptake of heroin injected intravenously is probably limited by the regional flow of blood in the brain. The possible relation of this rapid penetration of the blood-brain barrier by heroin to its strongly addictive properties is discussed.

Animals↗

Double-blind oral analgesic study of butorphanol in musculoskeletal pain: a comparison with codeine and placebo.

Butorphanol tartrate (4 mg and 8 mg) was compared to codeine phosphate (60 mg) and placebo for oral analgesic activity and side-effects employing a double-blind design in ninety-three out-patients suffering from moderate to very severe musculoskeletal pain. The study duration was 72 hours with medication administered every 4 to 6 hours (four times daily) for a total of twelve doses per patient. The results demonstrate that both the 4 mg and 8 mg doses of butorphanol were significantly better (p less than 0.u5) than placebo. While codeine 60 mg also proved active, it appears to be less efficacious than the high dose of butorphanol. The peak effect appeared to be evident in 1 to 2 hours. Butorphanol may be at least seven times more potent than codeine on a milligram basis. Although no serious side-effects were observed, butorphanol appeared to present a greater incidence of side-effects than codeine and placebo in this study.

Adolescent↗

Differential sensitivity to physical dependence on morphine and codeine in three inbred strains of mice.

The purpose of this experiment is to investigate genetic differences in the development of physical dependence on morphine and codeine in inbred strains of mice, C57BL/6, C3H/He and DBA/2. Mice were treated with morphine- or codeine-admixed food (1, 2 and 3 mg/g of food) for 3 to 9 days. After the termination of drug treatment, the mice were given naloxone (5 mg/kg, s.c.). The incidences of jumping and teeth chattering by naloxone challenge in morphine- and codeine-treated C57BL/6 mice were much greater than those in C3H/He and DBA/2 mice. However, the incidences of other naloxone-precipitated withdrawal signs, such as ptosis and diarrhea, were not different among the three inbred strains of mice. These results indicate that genotype is an important determinant of the degree of most naloxone-precipitated withdrawal signs in morphine- and codeine-treated mice.

Animals↗

Slow release polymer-drug systems obtained by moisture promoted polyreactions. 1. Codeine resinate encapsulated in poly(alkyl alpha-cyanoacrylates).

Samples of codeine resinate consisting of a carboxylic cation exchanger (as a polymeric carrier) and codeine (as a drug) were coated with poly(alkyl alpha-cyanoacrylates) by suspending and stirring wet resinate beads in a toluene solution of the monomer. Methyl, ethyl and n-butyl alpha-cyanoacrylates were used as monomers. Each coated material released codeine more slowly than the non-coated. The data obtained confirmed that water promoted the polymerization of alkyl alpha-cyanoacrylates, which proceeded at the surface of the wet resinate beads. The rate of codeine release depended on the type of monomer used for coating, the monomer/resinate feed ratio and the plymerization time.

Analgesics, Opioid↗

Gas-chromatographic measurement of codeine and norcodeine in human plasma.

A gas-chromatographic method is described for determination of codeine and norcodeine in human plasma. The method is specific, sensitive, and precise. It was developed for use in bioavailability studies of therapeutic doses of codeine sulfate. After ingestion of a 60-mg codeine sulfate tablet, mean peak codeine concentration in plasma was 107 mug/liter at 1.0 hour. No measurable concentration of norcodeine was found in the plasma by this method.

Chromatography, Gas↗

Increased urinary morphine, codeine and tetrahydropapaveroline in parkinsonian patient undergoing L-3,4-dihydroxyphenylalanine therapy: a possible biosynthetic pathway of morphine from L-3,4-dihydroxyphenylalanine in humans.

We have identified morphine and codeine in human urine by means of gas chromatography/mass spectrometry. Gas chromatography/mass spectrometry was also used to quantitate the two alkaloids and tetrahydropapaveroline (THP) in urine of both normal subjects and parkinsonian subjects receiving L-dopa therapy. The morphine, codeine and THP levels in healthy nondrinker controls were 2.93 +/- 0.23, 2.01 +/- 0.53 and 6.70 +/- 1.13 pmol/ml (mean +/- S.E.M.), respectively. In contrast, the urinary levels of codeine and THP in L-dopa-treated parkinsonian patients were significantly elevated to 62.20 +/- 17.54 and 31.04 +/- 15.69 pmol/ml, respectively. Some of the parkinsonian patients showed high urinary morphine levels. Morphine excretion was also enhanced in patients complaining of severe pain due to herpes zoster (24.60 +/- 9.51 pmol/ml) but not in patients with severe pain due to cerebral embolus. These alkaloid levels in the urine of abstinent alcoholics were very low. There were significant correlations among these three alkaloid levels in the urine. The results indicate that morphine and codeine are synthesized in the body from L-dopa and/or dopamine, via the THP-related pathway.

Adult↗

[Pilot study of the metabolism of codeine to morphine and a possible modification by benzodiazepines].

After administration of high-dose codeine we found that in two cases 20-40% of the total morphine-equivalents in the 24-hour urine sample were free morphine. After another 24 hours the proportion of free morphine was up to 70% and after roughly 96 hours even went up to 96%. Although 10% of the administered codeine was eliminated as morphine. In contrast to the values reported in literature we found that even with codeine/morphine ratios greater than 0.5 and morphine concentrations of up to 2000 ng/ml urine one cannot naturally conclude that morphine/diamorphine has been consumed. The short half-life of codeine in serum was 2-4 hours, the final half-life was 9-11 hours. In urine we found a short half-life of 1-6 hours as well as a long half-life of 7-12 hours. When diazepam was administered simultaneously with codeine the expected half-life in serum was up to 1.5 times and in urine 2.5 times. The codeine/morphine ratios were hardly affected so far as evidence goes which they give of preceding drug-intake.

Biotransformation↗

Effects of ephedrine and phenylpropanolamine on the antinociceptive effects of morphine and codeine in mice.

The effects of ephedrine and phenylpropanolamine on the antinociceptive activities of morphine and codeine were investigated. Both morphine and codeine exhibited dose-dependent antinociceptive activities in the tail flick test. Ephedrine (5, 10 and 20 mg/kg) and phenylpropanolamine (5, 10 and 20 mg/kg) showed no antinociceptive effect when administered alone. The antinociceptive effects of morphine were enhanced in mice pretreated with ephedrine or phenylpropanolamine. similarly, codeine antinociception was increased in mice pretreated with ephedrine or phenylpropanolamine. In all cases, the ED50 values and single dose comparisons were shifted in the same direction. These effects on the antinociceptive potencies of morphine and codeine were found to be dose-dependent, being statistically significant at the higher dose levels of ephedrine and phenylpropanolamine used in the present study.

Analgesics↗

[Antitussive effects of Bakumondô-tô and codeine in bronchitic guinea-pigs].

Antitussive effects of Bakumondô-tô and codeine were examined in bronchitic guinea-pigs made by an exposure to SO2. Bakumondô-tô significantly depressed the cough reflex induced by mechanical and chemical stimulations in the bronchitic but not in the normal animals. Repeated administration of Bakumondô-tô significantly suppressed the increased spontaneous discharge of the superior laryngeal nerve in bronchitic animals. On the other hand, the antitussive action of codeine in bronchitic animals was significantly weaker than that in normal animals. Moreover, repeated administrations of codeine significantly potentiated the increased spontaneous discharge of the superior laryngeal nerve. The results suggest that Bakumondô-tô, unlike codeine, has a notable antitussive activity in bronchitic rather than in normal guinea-pigs.

Animals↗

Antitussive action of the new anilide derivative vadocaine hydrochloride compared with codeine phosphate in four animal models.

Vadocaine hydrochloride (2',4'-dimethyl-6'-methoxy-3-(2-methylpiperidyl) propionanilide hydrochloride, OR K-242-HCl; INN: vadocaine) is a novel antitussive compound structurally resembling local anaesthetics. Its antitussive profile was studied in several animal models. In guinea-pigs, vadocaine reduced by about 70% the cough episodes induced by sulphur dioxide or ammonia. The effective dose was 2.5 mg/kg p.o., and codeine phosphate was less effective. In cats, vadocaine (3 mg/kg i.v.) inhibited by about 80% for 10 min the cough reflex initiated by mechanical irritation of the trachea. When vadocaine was given via the vertebral artery, it was about 10 times more active than by the intravenous route. Codeine was 3 times as active as vadocaine by both routes. This result indicates an important central component in the antitussive action of vadocaine. In another cat model, 5 mg/kg of vadocaine was somewhat weaker than 1 mg/kg of codeine in inhibiting the cough caused by electrical stimulation of the laryngeal nerve (Domenjoz' method). In dogs, both oral and intravenous doses of 6 mg/kg of vadocaine and 2 mg/kg of codeine were approximately equiactive, inhibiting by 60-80% the cough induced by electrical stimulation of the trachea. Concentrations of vadocaine in serum were around 1 microgram/ml during oral administration. By both routes, the antitussive activity (inhibition of cough by 50% or more) lasted at least 2 h. Vadocaine caused local anaesthesia in the guinea-pig wheal preparation at concentrations of 0.25% and 0.5%, and on the guinea-pig cornea at 0.5%. Duration of anaesthesia was longer than that of lidocaine. Vadocaine did not affect the guinea-pig tracheal strip preparation.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthetics, Local↗

Codeine-induced mast cell degranulation in human skin: effect of calcium channel blockers.

Codeine and other opiates can induce immediate type wheal and flare skin reactions. Calcium channel blockers including nifedipine have been shown to inhibit mast cell degranulation in different systems. The oral administration of nifedipine (10 mg) did not affect the size of codeine-induced skin reactions in ten normal volunteers. Mean wheal over flare sizes were 11.7 mm/29.2 mm before nifedipine and 11.5 mm/31.0 mm at peak nifedipine blood levels. Similar observations were made when codeine was injected locally with or without 20 micrograms nifedipine (12.1/29.2 mm and 13.2/29.2 mm, respectively). These data suggest that codeine-induced mast cell degranulation may be mediated by a calcium-independent mechanism. Alternatively, mast cells in the human skin may differ in their reactions to secretagogues when compared with basophils and mast cells from other human tissues or other species.

Adult↗

[Relative bioavailability of paracetamol from tablets and suppositories as well as of paracetamol and codeine in a combination tablet].

Eight healthy male volunteers took part in this study to determine the relative bioavailability of Treuphadol oblong tablets (500 mg paracetamol), Treuphadol Plus oblong tablets (500 mg paracetamol, 30 mg codeine phosphate) and Treuphadol suppositories (750 mg paracetamol) against commercial tablets (500 mg paracetamol). Plasma levels of paracetamol and codeine, plus saliva levels of paracetamol for the two paracetamol only formulations, were determined by HPLC and the pharmacokinetic parameters established. The AUC data for paracetamol showed that all four preparations were bioequivalent. The saliva levels of paracetamol demonstrated a good correlation to the corresponding plasma levels. The pharmacokinetic data of codeine from the Treuphadol Plus tablet were compared with corresponding data from the literature. The bioequivalence of codeine when based on this comparison can also be assured.

Acetaminophen↗

Concentrations of morphine and codeine in serum and urine after ingestion of poppy seeds.

We measured morphine and codeine in commercially available poppy seeds and in serum and urine samples from healthy adults who had ingested these poppy seeds. Four brands of black poppy seeds, examined by gas chromatography-mass spectroscopy (GC-MS) with deuterated internal standards, contained from 17 to 294 micrograms of morphine and 3 to 14 micrograms of codeine per gram of seeds. Morphine was detected by GC-MS in hydrolysates of serum as late as 24 h after ingestion, with a maximum mean concentration of 100 ng/mL (range 82-131) measured 2 h after the subjects ingested 25 g of seeds. Opiates were detectable (greater than 300 micrograms/L) in urine by enzyme-multiplied immunoassay (EMIT; Syva Co.) and by radioimmunoassay screening procedures for as long as 48 h after ingestion. The identity and quantities of morphine and codeine in poppy seed extracts and in hydrolysates of serum and urine were confirmed by GC-MS. Therefore a positive finding of morphine or codeine in blood and urine may sometimes be due to ingestion of poppy seeds.

Codeine↗

Potentiation of antitussive effect of codeine by some 1-dimethoxyphenyl-3-alkylaminobutanols in guinea pigs.

Newly synthesized 1-(2',5'-dimethoxyphenyl)-1-n-butyl-3-diethylaminobutanol (compd. 4) and its analogs enhanced the antitussive effect of codeine and morphine as tested on the cough induced by mechanical stimulation of the trachea in guinea pigs. This effect was illustrated to be a potentiation on the Gaddum's diagram. The following parameters were affected little or to a small extent: 1. analgesic effect of codeine and morphine in guinea pigs and mice, 2. duration of anesthesia induced by hexobarbital in mice, 3. respiratory depression caused by codeine in guinea pigs, and 4. LD50 of codeine in guinea pigs and mice. Explorations of the mechanism of potentiating action suggested some peripheral mechanism, but the exact one remained to be elucidated.

Amino Alcohols↗

Deaths related to propoxyphene or codeine or both.

Ninety-nine deaths involving propoxyphene or codeine or both were investigated through interviews with surviving relatives and associates. The criterion for admission to this study was the presence of propoxyphene or codeine in the body fluids or tissues, determined analytically. The codeine-related group included more ethnic minority persons, more histories of primary drug addiction, more users of street drugs, and more accidental deaths. In the propoxyphene-related group there were fewer histories of drug addiction and more persons with mental illness and more suicides. Most victims had considerable past experience with one or both of the drugs and other drugs as well. Propoxyphene was usually obtained by physician prescription. Codeine was often obtained illegally.

Adult↗

Double-blind cross-over study comparing loperamide, codeine and diphenoxylate in the treatment of chronic diarrhea.

As no adequate comparison of these widely used drugs has been made, we have performed a double-blind cross-over trial in 30 individuals with chronic diarrhea. Each underwent three randomized treatment periods of 4 wk duration. Patients were instructed to increase the daily dose gradually until control was achieved or side effects became intolerable. Stool frequency, consistency, urgency, and incontinence were then compared when a stable dose was reached. Though 2.3 capsules (4.6 mg) of loperamide, 2.3 capsules (103.5 mg) of codeine and 2.5 capsulses (12.5 mg) of diphenoxylate all reduced stool frequency to the same extent, diphenoxylate was significantly less effective in producing a solid stool. Before treatment 95% of patients experienced urgency, sometimes associated with fecal incontinence, often as their major diability. Loperamide and codeine were more effective in relieving this than was diphenoxylate. Side effects, particularly central nervous effects, were greatest with diphenoxylate and least with loperamide. Approximately equal numbers discontinued each preparation; poor control and central-nervous-system side effects were the usual reasons for stopping diphenoxylate and codeine, and abdominal pain and constipation for stopping loperamide. We conclude that both loperamide and codeine phosphate are superior to diphenoxylate in the symptomatic treatment of chronic diarrhea.

Antidiarrheals↗

[Biopharmaceutic properties of slow-release codeine phosphate. Drug release from ion exchangers in vitro and in vivo].

The release of bound codeine (CAS 76-57-3) from a cation exchanger was examined in vitro by the flow-through method and in vivo by measuring the plasma concentrations of codeine after administration of slow-release (Codipront Retard) and standard non-retarded drops. Both sets of results show that codeine release from the ion exchanger is protracted and continuous. Relative to the standard formulation the slow-release codeine drops give a lower maximal plasma concentration (Cmax), a delayed time of maximal concentration (tmax), slower absorption (t0.5) and protracted plasma levels. The in vitro and in vivo results were in good agreement.

Adult↗