Methcathinone Intoxication in the Rat: Abrogation by Dextrorphan

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 w...

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Bibliographic Details
Published in:	Annals of emergency medicine Vol. 29; no. 3; pp. 383 - 391
Main Authors:	Rockhold, Rob W, Carlton, Fredrick B, Corkern, Robert, Derouen, Len, Bennett ‡, James G, Hume, Arthur S
Format:	Journal Article
Language:	English
Published:	New York, NY Mosby, Inc 01-03-1997 Elsevier
Subjects:	Animals Biological and medical sciences Designer Drugs - toxicity Dextrorphan - administration & dosage Dextrorphan - pharmacology Drug addictions Fever - chemically induced Lethal Dose 50 Male Medical sciences Propiophenones - antagonists & inhibitors Propiophenones - toxicity Rats Rats, Sprague-Dawley Receptors, Amino Acid - antagonists & inhibitors Seizures - chemically induced Tachycardia - chemically induced Time Factors Toxicology Rat Toxicity Drug intoxication Rodentia Cathinone Toxicology Vertebrata Alkaloid Mammalia Aminoacid Animal Antagonist Hemodynamics Antidote Dextrorphan
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Summary:	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° 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°±.3° 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. [Rockhold RW, Carlton FB, Corkern R, Derouen L, Bennett JG, Hume AS: Methcathinone intoxication in the rat: Abrogation by dextrorphan. Ann Emerg Med March 1997;29:383-391.]
ISSN:	0196-0644 1097-6760
DOI:	10.1016/S0196-0644(97)70351-2