A placebo-controlled treatment trial in 26 cocaine-addicted subjects aimed to determine whether dexmedetomidine reverses MAP and HR increases after intranasal cocaine (3 mg/kg).
Key Findings
Low-dose dexmedetomidine (0.4 µg/kg) abolished cocaine-induced increases in MAP (+6 ± 1 versus -5 ± 2 mm Hg; P<0.01), but had no effect on HR (+13 ± 2 versus +9 ± 2 bpm; P=ns).
Skin sympathetic nerve activity and skin vascular resistance were significantly reduced.
A higher sedating dose of dexmedetomidine (1.0 μg/kg) was needed to counteract the modest HR rise, but at the expense of increasing BP in one third of patients.
Application to Clinical Practice
In a low nonsedating dose, dexmedetomidine may be a potential (adjunct) treatment for cocaine-induced acute hypertension. However, higher sedating doses can increase blood pressure unpredictably during acute cocaine challenge and should be avoided.
Generous benzodiazepine should remain first-line therapy.
References
Kontak AC, et al. Dexmedetomidine as a Novel Countermeasure for Cocaine-Induced Central Sympathoexcitation in Cocaine-Addicted Humans. Hypertension 2013;61(2):388-94. [PMID 23283356].
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