This chapter focuses on cocaine overdose, discussing its effects on the peripheral circulation. Cocaine addiction is increasing worldwide among all income strata. Cocaine is the most common illicit drug causing life-threatening cardiovascular emergencies, including acute coronary syndrome, stroke, sudden cardiac death, hypertensive crisis, and aortic dissection. Inhibition of the NE transporter in the peripheral circulation cannot be the only mechanism by which cocaine acutely raises blood pressure. Tricyclic antidepressants, which are more potent NE transporter inhibitors than cocaine, do not raise blood pressure. Although microneurographic measurements of cardiac sympathetic nerve activity (SNA) are not possible to perform in human subjects, our microneurographic studies show that intranasal cocaine is a potent stimulus to skin SNA, a regional sympathetic outflow that is very sensitive to central neural stimuli but quite insensitive to baroreflex stimuli. Hyperthermia is a specific complication of cocaine overdose, which further amplifies the drug's cardiovascular toxicity. The precise mechanism by which cocaine impairs both cutaneous vasodilation and sweating is still unknown but likely has a central mechanism of action because heat perception was also impaired by cocaine.
|Original language||English (US)|
|Title of host publication||Primer on the Autonomic Nervous System|
|Number of pages||5|
|State||Published - Dec 1 2012|
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