From: "Kroll, Mark W." <MKroll@sjm.com>
Date: Wed Feb 12, 2003 6:53:36 PM America/Phoenix
To: "'Rick@taser.com'" <Rick@taser.com>
Subject:
Pharmacotherapy 1996 May-Jun;16(3):429-37
<http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?db=PubMed&cmd=Display&dopt=pubmed_pubmed&fr
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The effect of cocaine on Ventricular fibrillation threshold in the
normal canine heart
Tisdale JE, Shimoyama H, Sabbah HN, Webb CR.
College of Pharmacy and Allied Health Professions, Wayne State University, Detroit, MI 48202,
USA.
We determined the effect of cocaine on ventricular vulnerability to fibrillation, as measured by ventricular
fibrillation threshold (VFT), and cardiac electrophysiology in 20 anesthetized dogs with normal hearts.
Animals were randomized in blinded fashion to receive a continuous 3-hour infusion of cocaine 0.11
mg/kg/minute (total dose 20 mg/kg) or placebo (lactose dissolved in normal saline). The VFT, systolic and
diastolic blood pressures, ventricular effective refractory period (ERP), and electrocardiographic intervals
were measured at baseline and every 30 minutes during infusion. Baseline mean +/- SE VFT in cocaine
and placebo groups was 57.0 +/- 7.8 and 51.8 +/- 7.6 mA, respectively (p = 0.64). Cocaine did not
significantly decrease VFT, but actually increased it (i.e., reduced ventricular vulnerability to fibrillation)
compared with placebo (84.6 +/- 10.4 vs 55.8 +/- 7.2 mA, respectively, at 150 minutes, p = 0.04). Cocaine
prolonged ERP and PR, QRS, QT, QTc, JT, and JTc intervals. Cocaine does not increase ventricular
vulnerability to fibrillation in anesthetized dogs with normal intact hearts. Its electrophysiologic effects are
similar to those of class I antiarrhythmic agents in this model.
Mark W. Kroll, PhD, FACC
Senior Vice President
Chief Technology Officer
St. Jude Medical, Inc.
Cardiac Rhythm Management Division
15900 Valley View Court
Sylmar, CA 91342
Voice: +1-818-493-2234