Circulation, Vol 76, 1397-1408, Copyright © 1987 by American Heart Association
KM Wu and BF Hoffman
We studied the effects of procainamide and N-acetylprocainamide (NAPA) in a
conscious dog preparation of atrial flutter resulting from circus movement
around the tricuspid orifice. We also recorded transmembrane potentials of
atrial tissues from the circus path in vitro. In 12 instrumented dogs,
average flutter cycle length was 157 msec, the duration of the excitable
gap was 73 msec, and conduction velocity was 0.75 m/sec. At 4 and 8 mg/kg,
procainamide moderately prolonged cycle length, but did not terminate the
flutter. At a cycle length of 300 msec procainamide increased effective
refractory period (ERP) by 12% and 20% and conduction time by 8% and 19%.
At 16 and 32 mg/kg procainamide prolonged cycle length, ERP, and conduction
time by 60% to 80% and stopped the flutter in all trials. NAPA, at 16, 32,
and 64 mg/kg, increased flutter cycle length by 16%, 16%, and 31%, ERP by
14%, 28%, and 41%, and conduction time by less than 15%. NAPA terminated
the flutter in two of six dogs given 32 mg/kg, and three of five dogs given
64 mg/kg. The excitable gap was lengthened by both procainamide and NAPA.
Transmembrane potentials showed that at a cycle length from 1000 to 300
msec procainamide (10 mg/liter) increased action potential duration and
decreased the first time derivative of phase O of the action potential
(Vmax), whereas NAPA (20 mg/liter) increased action potential duration
without changing Vmax. These findings show the difficulty of relating drug
effects on transmembrane potentials to efficacy in vivo since the former do
not necessarily indicate which changes in cellular electrical activity are
responsible for efficacy against a particular arrhythmogenic mechanism.
ARTICLES
Effect of procainamide and N-acetylprocainamide on atrial flutter: studies in vivo and in vitro
Department of Pharmacology, College of Physicians and Surgeons, Columbia University, New York, NY 10032.
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