ethylmorphine and dihydrocodeine

An opioid tramadol more effectively inhibits compound action potentials (CAPs) than its metabolite mono-O-demethyl-tramadol (M1). To address further this issue, we examined the effects of opioids (morphine, codeine, ethylmorphine and dihydrocodeine) and cocaine on CAPs by applying the air-gap method to the frog sciatic nerve. All of the opioids at concentrations less than 10 mM reduced the peak amplitude of the CAP in a reversible and dose-dependent manner. The sequence of the CAP peak amplitude reductions was ethylmorphine>codeine>dihydrocodeine> or = morphine; the effective concentration for half-maximal inhibition (IC(50)) of ethylmorphine was 4.6 mM. All of the CAP inhibitions by opioids were resistant to a non-specific opioid-receptor antagonist naloxone. The CAP peak amplitude reductions produced by morphine, codeine and ethylmorphine were related to their chemical structures in such that this extent enhanced with an increase in the number of -CH(2) in a benzene ring, as seen in the inhibitory actions of tramadol and M1. Cocaine reduced CAP peak amplitudes with an IC(50) value of 0.80 mM. It is concluded that opioids reduce CAP peak amplitudes in a manner being independent of opioid-receptor activation and with an efficacy being much less than that of cocaine. It is suggested that the substituted groups of -OH bound to the benzene ring of morphine, codeine and ethylmorphine as well as of tramadol and M1, the structures of which are quite different from those of the opioids, may play an important role in producing nerve conduction block.

Topics: Action Potentials; Analgesics, Opioid; Animals; Calcium Channels; Cocaine; Codeine; Ethylmorphine; Female; Male; Morphine; Naloxone; Potassium Channels, Voltage-Gated; Ranidae; Receptors, Opioid; Sciatic Nerve; Structure-Activity Relationship; Tetrodotoxin

We describe a method using a gas chromatograph with electron ionization detection (GCD) for the simultaneous determination of morphine, codeine, 6-monoacetylmorphine, ethylmorphine, and dihydrocodeine in blood. The method employs propionic anhydride in the presence of triethylamine to propionylate free hydroxyl groups of the opiates in blood. The quantitation is achieved by using GCD with selected ion monitoring of the two most characteristic ions for each analyte. The quantitation limit was 0.01 mg/L and the linearity was 0.01-10 mg/L for dihydrocodeine, ethylmorphine, and 6-monoacetylmorphine. For the other investigated opiates, the quantitation limit was 0.025 mg/L and linearity was 0.025-10 mg/L. The intraday relative standard deviation (RSD) varied from 7.2 to 10% at the 0.5 mg/L level, and the day-to-day RSDs varied from 7.5 to 11% at the 0.85 mg/L level.

Topics: Anhydrides; Codeine; Ethylamines; Ethylmorphine; Gas Chromatography-Mass Spectrometry; Humans; Morphine; Morphine Derivatives; Narcotics; Propionates; Reproducibility of Results; Substance Abuse Detection

A fatal opiates overdose, where ethylmorphine, hydrocodone, dihydrocodeine and codeine were consumed concomitantly, is reported. This case report may contribute to data on fatal blood concentrations of drugs with rare incidence. The relative retention times in capillary gas chromatography and full mass spectra of various opiates in their silylated forms, detected together in one sample, may serve as a helpful analytical reference for clinical and forensic toxicologists.

Topics: Adult; Codeine; Drug Overdose; Ethylmorphine; Fatal Outcome; Gas Chromatography-Mass Spectrometry; Humans; Hydrocodone; Male; Opioid-Related Disorders; Toxicology