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At least 469 records · Page 26Linked to original sources
PubMed1986

Intrathecal injection of codeine, buprenorphine, tilidine, tramadol and nefopam depresses the tail-flick response in rats.

The effect of intrathecal (i.t.) injection of the analgesic agents, codeine, buprenorphine, tilidine and one of its metabolites, nortilidine, tramadol and nefopam, was determined in the tail-flick test performed on rats. ED50 values were derived from the dose-response lines. The relative potency ranking established from the ED50 values is buprenorphine (0.4 nM) greater than nortilidine (29 nM) = tramadol (26 nM) = nefopam (34 nM) greater than codeine (42 nM) greater than tilidine (118 nM). An i.t. injection of the opiate antagonist, naloxone (5 micrograms), prevented the antinociceptive effect of all analgesic agents administered at the highest dose tested. It is concluded that these analgesic agents, like morphine, exert their effect at least in part through a spinal site of action.

Analgesics↗
PubMed1987

Morphine and codeine are endogenous components of human cerebrospinal fluid.

We have examined cerebrospinal fluid (CSF) from twelve patients who were not on any medication and found them to contain both morphine and codeine in concentrations of 2 to 339 fmol/ml. These are comparable to the concentration of opioid peptides in spinal fluid. Both morphine and codeine are present mainly in conjugated form from which the free alkaloids can be released by acid hydrolysis.

Adolescent↗
PubMed1995

Affinity profiles of morphine, codeine, dihydrocodeine and their glucuronides at opioid receptor subtypes.

The affinity of morphine, codeine, dihydrocodeine and their glucuronides for mu-, delta-, and kappa-opioid receptors was investigated. Binding was studied on guinea-pig brain homogenates with [3H]DAMGO, [3H]DPDPE, and [3H]U69593. The substitution of the free phenolic group of morphine caused a decrease in binding at opioid receptors without affecting the mu/delta-ratio nor that of mu/kappa. Glucuronidation of the 6-hydroxyl group of morphine, codeine or dihydrocodeine did not affect the affinity to mu-receptors, slightly increased the affinity for delta-receptors and reduced the affinity for kappa-receptors. The 6-glucuronides possess a decreased selectivity for mu-receptors over delta-receptors whereas that for mu- over kappa-receptors was increased. It is concluded that chemical variations at 3- and 6-position of morphine independently affect the affinity to opioid receptor subtypes.

Animals↗
PubMed1995

Possible role of endogenous morphine and codeine on growth regulation of lung tissue.

The literature indicates that morphine can inhibit the growth of both small cell and non small cell lung cancer cell lines and that nicotine can reverse this inhibition. In this report we present data showing that mammalian lung tissue contain the opiate alkaloids morphine and codeine and that these alkaloids are also to be found in normal lung cell lines. However, analysis of both small cell and non small cell lung cancer cells indicate that they do not contain these opiate alkaloids endogenously. If morphine exerts an inhibitory effect on proliferation of these cells it is interesting that the lung cancer cell lines lack the opiate alkaloids endogenously. Our studies also present data indicating that the circulating levels of morphine and codeine are elevated in smokers as compared to non smokers which we hypothesize to reflect the invocation of a compensatory mechanism.

Adult↗
PubMed1990

Studies of the mechanism of angiotensin-converting enzyme (ACE) inhibitor-associated angioedema: the effect of an ACE inhibitor on cutaneous responses to bradykinin, codeine, and histamine.

To understand better the mechanism of angiotensin-converting enzyme (ACE) inhibitor-associated angioedema, we studied the effects of ACE-inhibitor treatment on wheal-and-flare responses to histamine, codeine, and bradykinin in 10 normal subjects. No change in the size of wheal-and-flare reactions to histamine occurred, but the size of wheal reactions to codeine and bradykinin increased in all study subjects after ingesting the ACE inhibitor, captopril. Five of 10 study subjects developed flushing reactions after ACE-inhibitor treatment. We conclude that inhibition of bradykinin metabolism by ACE inhibitors is the probable cause of ACE inhibitor-related angioedema and that substance P is not the predominant mediator in this process.

Adult↗
PubMed1991

Abuse of "BRON": a Japanese OTC cough suppressant solution containing methylephedrine, codeine, caffeine and chlorpheniramine.

1. The paper describes the mental disturbances of 44 abusive cases of "BRON," an over-the-counter (OTC) cough suppressant solution containing methylephedrine, codeine, caffeine, and chlorpheniramine. 2. Major psychiatric symptoms observed included hallucinatory-paranoid state and affective disorder. There also were groups which exhibited a combination of the two states and abuse only. 3. The hallucinatory-paranoid state group had a relatively small BRON usage amount, short usage term and few withdrawal symptoms. The affective disorder group, in contrast, had large usage amount, longer usage term, and showed significant autonomic nerve disorders during withdrawal. These tendencies were seen more clearly in the mixed state group. 4. The hallucinatory-paranoid state group showed little or no physical dependence, while that of the affective disorder group was thought to be firmly established. Thus, in the former group, methylephedrine was considered the major behavior modifying drug, while in the latter, it was thought to be codeine.

Adult↗
PubMed1989

Toxicity studies of amphetamine sulfate, ampicillin trihydrate, codeine, 8-methoxypsoralen, alpha-methyldopa, penicillin VK and propantheline bromide in rats and mice.

Thirteen-week toxicity studies in F344/N rats and B6C3F1 mice were conducted to determine general toxicity and target organ toxicity with amphetamine sulfate, ampicillin trihydrate, codeine, 8-methoxypsoralen, alpha-methyldopa sesquihydrate, penicillin VK, and propantheline bromide. This paper discusses the toxicity observed; use of the toxicity data to set dose levels for subsequent 2-year studies; and comparison of dose levels administered to rodents with doses used in the treatment of human disease. Drugs were administered orally in the feed or by gavage. The lowest doses in the 13-week studies were comparable to therapeutic doses in man on a mg/m2 (body surface area) basis or 5-10 times doses used in man on a mg/kg body weight basis. Little toxicity was seen at the low dose level with ampicillin, penicillin VK, 8-methoxypsoralen or propantheline bromide. At higher doses, target organ toxicity seen included the urinary bladder in male rats after propantheline bromide; the glandular stomach in rats and mice after penicillin VK; the liver and adrenals in rats after 8-methoxypsoralen; and the kidney in mice and rats after alpha-methyldopa. After amphetamine, codeine, or ampicillin administration, no target organ toxicity was seen in rats or mice, even at doses which caused body weight gain depression. The high doses chosen for subsequent 2-year studies were within 10 times human dose levels when compared on a mg/m2 body surface area.

Ampicillin↗
PubMed1996

Decreased incidence of spontaneous mammary gland neoplasms in female F344 rats treated with amphetamine, methylphenidate, or codeine.

Three drugs that affect the neuroendocrine system (amphetamine, methylphenidate, and codeine) caused decreases in body weights and in the incidence of spontaneously occurring mammary gland neoplasms in the female F344/N rat in 2-year carcinogenicity studies. Using a mathematical model that relates body weight changes to the incidence of mammary gland neoplasms, we find that the decrease in mammary gland tumours seen in female rats cannot be fully explained by body weight decreases relative to control animals. Further, the observed decreases in body weight in treated female rats were not a function of differences in feed consumption between treated and control groups. These pharmaceuticals are thought to affect the biologic system through interaction with membrane receptors. This interaction and/or subsequent cell signaling events may play a role in the observed decrease in spontaneously occurring mammary gland neoplasms in the female rat treated with amphetamine, methylphenidate, or codeine.

Amphetamine↗
PubMed1992

Brain and adrenal monoamines and neuropeptide Y in codeine tolerant rats.

1. Monoamine turnover and neuropeptide Y (NPY) levels were investigated in the central and peripheral nervous systems in adult male rats chronically treated with codeine. 2. An increase in the dopaminergic turnover was observed in the striatum and cortex. The norepinephrine levels and the serotoninergic turnover were unchanged in all the brain areas. 3. Epinephrine levels were decreased in the adrenal glands. 4. In addition, we observed a significant decrease of NPY levels in the hypothalamus, the striatum and the adrenal glands. These observed changes were not found when assessing NPY level in plasma fluid. 5. The implication of these modifications in the induction of codeine dependence are discussed in view of previous results obtained with morphine.

Adrenal Glands↗
PubMed1993

Simultaneous determination of 6-monoacetylmorphine, morphine and codeine in urine using high-performance liquid chromatography with combined ultraviolet and electrochemical detection.

A method is described for the simultaneous determination of 6-monoacetylmorphine (6-MAM), morphine and codeine in post-mortem urine specimens using reversed-phase high-performance liquid chromatography with dual ultraviolet spectrophotometric and electrochemical detection. The limits of detection for a 1-ml urine sample were 0.04 mg/l for 6-MAM and 0.05 mg/l for both morphine and codeine. The presence of 6-MAM in urine indicates prior use of heroin and enables differentiation between morphine- and heroin-related deaths.

Chromatography, High Pressure Liquid↗
PubMed1987

The illicit preparation of morphine and heroin from pharmaceutical products containing codeine: 'homebake' laboratories in New Zealand.

Since 1983 a large number of small-scale illicit laboratories producing morphine and heroin from commercially available, codeine-based pharmaceutical products have been encountered in New Zealand. The codeine demethylation procedure is based on the use of pyridine hydrochloride. Very simple laboratory equipment and reagents are required and these can be utilised by people with little or no chemical background, following a recipe-like procedure. The process yields a characteristic product known as 'homebake'. This process is fully described.

Chemical Phenomena↗
PubMed1995

Analysis of unconjugated morphine, codeine, normorphine and morphine as glucuronides in small volumes of plasma from children.

A sensitive method for the analysis of unconjugated morphine, codeine, normorphine and total morphine after hydrolysis of glucuronide conjugates is described. The method was applicable to 50-microliters volumes of plasma. The analytes were converted to heptafluorobutyryl (HFB) derivatives before analysis by gas chromatography-negative ion chemical ionization mass spectrometry. Morphine and codeine were quantified against their [2H3]-isotopomers. Linearity, precision and accuracy were quite acceptable (in the 10(-10)-10(-9) g range), and the absolute limits of detection were < 1 pg.

Child↗
PubMed1987

Studies on the effects of the narcotic alkaloids, cocaine, morphine, and codeine on nonenzymatic lipid peroxidation in rat brain mitochondria.

This paper presents evidence of studies on the effects of the narcotic alkaloids, cocaine hydrochloride, morphine sulfate, and codeine phosphate, on nonenzymatic lipid peroxidation in rat brain mitochondria. These organelles abound in polyunsaturated fatty acids and are thus susceptible to oxidative attack. Lipid peroxidation was indexed mainly by assaying the extent of malonaldehyle (MDA) production and also the formation of fluorescent products in the course of the reaction. We found that morphine sulfate lowered fluorescence while the other two alkaloids showed no effect on lipid peroxidation in the absence of the inducers, 1.0 mM ascorbic acid or 0.1 mM ferrous sulfate. The apparent antioxidative nature of morphine sulfate was also observed in its effects on induced and noninduced MDA production, both cocaine hydrochloride and codeine phosphate stimulated MDA production by about 20% in the absence of any inducers. This paper also attempts to draw a structure-activity relationship for the antioxidative action of opium alkaloids, which we postulated to be due to the chelating capability of the alkaloid molecule.

Alkaloids↗
PubMed2000

Analysis of codeine, dihydrocodeine and their glucuronides in human urine by electrokinetic capillary immunoassays and capillary electrophoresis-ion trap mass spectrometry.

Screening for and confirmation of illicit, abused and banned drugs in human urine is a timely topic in which capillary separation techniques play a key role. Capillary electrophoresis (CE) represents the newest technology employed in this field of analysis. Two rapid competitive binding, electrokinetic capillary-based immunoassays are shown to be capable of recognizing the presence, but not the identity, of urinary opioids, namely codeine (COD), codeine-6-glucuronide, dihydrocodeine (DHC), dihydrocodeine-6-glucuronide, morphine (MOR), morphine-3-glucuronide and ethylmorphine (EMOR). In these approaches, aliquots of urine and immunoreagents of a commercial, broadly cross-reacting fluorescence polarization immunoassay for opiates were combined and analyzed by capillary zone electrophoresis or micellar electrokinetic capillary chromatography with laser induced fluorescence detection. With the fluorescent tracer solution employed, the former method is shown to provide simple electropherograms which are characterized by an opioid concentration dependent magnitude of the free tracer peak. In presence of dodecyl sulfate micelles, however, two tracer peaks with equal opioid concentration sensitivity are monitored. These data suggest the presence of two fluorescent tracers which react competitively with the urinary opioids for the binding sites of the antibody. Assay sensitivities for COD and MOR are comparable (10 ng/ml), whereas those for DHC and EMOR are about four-fold lower. Furthermore, glucuronides are shown to react like the corresponding free opioids. Analysis of urines that were collected after administration of 7 mg COD and 25 mg DHC tested positively in both assay formats. The presence of the free and conjugated codeinoids in these urines and their identification was accomplished by capillary electrophoresis-ion trap mass spectrometry (CE-MS). This confirmatory assay is based upon solid-phase extraction using a mixed-mode polymer cartridge followed by CE hyphenated to the LCQ mass spectrometer with electrospray ionization in the positive ion mode. With this technology, MS2 is employed for proper identification of COD (m/z 300.4) and DHC (m/z 302.4) whereas MS3 provides unambiguous identification of the glucuronides of COD (m/z 476.5) and DHC (m/z 478.5) via their fragmentation to COD and DHC, respectively. MSn (n > or = 2) is shown to be capable of properly identifying the urinary codeinoids on the 100-200 ng/ml concentration level.

Chromatography, Micellar Electrokinetic Capillary↗
PubMed1978

Rapid and sensitive gas chromatographic quantitation of morphine codeine and O6-acetylmorphine in illicit heroin using an electron capture detector.

Morphine, codeine and O6-acetylmorphine are reacted with heptafluorobutyric anhydride, rendering them suitable for electron capture detection and quantitation. The fluorinated derivatives are extracted from an acetonitrile-sodium bicarbonate solution into light petroleum in a rapid one-step extraction procedure. The derivatives are chromatographed on a stationary phase of 3% OV-17 on Gas-Chrom Q. Morphine, codeine and O6-acetylmorphine can be readily quantitated in heroin at levels as low as 0.001%, 0.01% and 0.01% respectively. Reproducibility, linearity and recovery studies are described.

Chromatography, Gas↗
PubMed2002

A rapid GC-MS method for the determination of dihydrocodeine, codeine, norcodeine, morphine, normorphine and 6-MAM in urine.

The presence of the heroin metabolite 6-monoacetylmorphine (6-MAM) in urine is used to definitively identify recent heroin abuse. A rapid and sensitive GC-MS method for the simultaneous analysis of codeine, norcodeine, morphine, normorphine and 6-MAM in urine was developed and successfully applied to the analysis of 321 'heroin-positive' urine specimens from individual subjects (identified by the presence of 6-MAM), to provide quantitative urinary opiate excretion data for heroin abusers. The cohort analysed was composed of 238 males (age range 16-53 years) and 83 females (age range 16-50 years). The concentrations of free 6-MAM, morphine and codeine determined in these 321 specimens ranged between 103-246,312, 129-193,600 and 103-519,000 microg/l, respectively. Free norcodeine and normorphine concentrations were found to range between 143-50,200 and 205-149,700 microg/l, respectively. A statistically significant relationship was determined between the subject age and the 6-MAM concentration, possibly indicating opiate tolerance in these individuals.

Adolescent↗
PubMed2001

Simultaneous determination of codeine and ethyl morphine HCL in tablet formulations using LC.

A reverse phase high performance liquid chromatography (HPLC) method was developed for the simultaneous determination of codeine (methyl morphine) and dionin (ethyl morphine hydrochloride) in antitussive analgesic tablet formulations. A C(18) column and methanol-water (1:2) mixture mobile phase (pH 3.0) were used. Spectrophotometric detection was carried out at 210 nm. The total elution time was shorter than 7 min. This method was found to be quite precise and reproducible. This proposed method was successfully applied to the determination of codeine and ethyl morphine hydrochloride in tablets produced by the Turkish Army Drug Factory.

Chromatography, High Pressure Liquid↗
PubMed1998

TLC-UV densitometric and GC-MSD methods for simultaneous quantification of morphine and codeine in poppy capsules.

Thin-layer chromatographic (TLC)-UV densitometric and gas-chromatographic-mass spectrometric detection (GC-MSD) methods were developed for simultaneous quantification of morphine and codeine in poppy capsules (Papaver somniferum). Morphine and codeine were isolated by extraction with chloroform: isopropanol (3:1, v/v) at pH = 8.5 and by solid-phase extraction on Snap-Cap cartridges at pH = 8.5. The TLC-UV densitometric quantification was performed by external standard method on silica gel plates using ethyl acetate: toluene: methanol: ammonia (68:17:10:5, v/v) as developing solvent and UV detection at 275 nm. For the GC-MSD analysis, the drugs were derivatized with acetic anhydride: pyridine (1:1, v/v) and separated on a 30 m HP5 capillary column. The quantification was performed using nalorphine as internal standard.

Analgesics, Opioid↗