Mechanisms of Acute Cocaine Toxicity
Kennon Heard*, 1, 2, Robert Palmer 1, Nancy R. Zahniser 3
Identifiers and Pagination:Year: 2008
First Page: 70
Last Page: 78
Publisher Id: TOPHARMJ-2-70
Article History:Received Date: 25/6/2008
Revision Received Date: 7/7/2008
Acceptance Date: 14/07/2008
Electronic publication date: 8/8/2008
Collection year: 2008
open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: https://creativecommons.org/licenses/by/4.0/legalcode. This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Patients with acute cocaine poisoning present with life-threatening symptoms involving several organ systems. While the effects of cocaine are myriad, they are the result of a limited number of cocaine-protein interactions, including monoamine transporter, neurotransmitter receptor and voltage-gated ion channels. These primary interactions trigger a cascade of events that ultimately produce the clinical effects. The purpose of this article is to review the primary interactions of cocaine and the effects that these interactions trigger. We also describe the progression of symptoms observed in cocaine poisoning as they relate to serum cocaine concentrations.