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Ann Emerg Med. 1997 Mar;29(3):383-91.

Methcathinone intoxication in the rat: abrogation by dextrorphan.

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  • 1Department of Emergency Medicine, University of Mississippi Medical Center, Jackson.

Abstract

STUDY OBJECTIVE:

Methcathinone, a designer drug, has high abuse liability. In this study we characterized acute methcathinone toxicity in rats, attempting to determine whether the excitatory amino acid receptor antagonist dextrorphan can antagonize methcathinone intoxication.

METHODS:

Intoxication was produced with IV methcathinone infusion (5 mg/kg/minute; 100 mg/mL) in conscious rats. We studied pretreatment, in which dextrorphan or vehicle was injected 30 minutes before methcathinone infusion. In a second protocol, dextrorphan or saline solution was given immediately after the onset of convulsions.

RESULTS:

Methcathinone caused tachycardia (maximal increase, 131 +/- 10 beats/minute), hyperthermia (+2.3 degrees C), convulsions, and cardiorespiratory collapse in vehicle-pretreated rats (n = 9). Death occurred after 32.0 +/- 1.1 minutes of infusion. Dextrorphan pretreatment (25 mg/kg; n = 7) significantly reduced hyperthermia (+.1 degree +/- .3 degree C) and tachycardia and increased the convulsive (dextrorphan, 134 +/- 9 mg/kg; vehicle, 67 +/- 4 mg/kg) and lethal doses (dextrorphan, 204 +/- 9 mg/kg; vehicle, 160 +/- 5 mg/kg). Dextrorphan, given immediately after the initial methcathinone convulsion, reduced hyperthermic and tachycardic responses but not the lethality of methcathinone.

CONCLUSION:

Blockade of excitatory amino acid receptors by dextrorphan minimizes acute methcathinone intoxication.

PMID:
9055779
[PubMed - indexed for MEDLINE]
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