Circulation, Vol 73, 1342-1353, Copyright © 1986 by American Heart Association
XT Shen and C Antzelevitch
The effects of therapeutic levels of quinidine were studied in an ischemic
gap preparation of reflected reentry. The preparation consisted of a
Purkinje fiber mounted in a three-compartment chamber. A narrow central
compartment was perfused with a solution prepared to mimic the
extracellular milieu at a site of ischemia. Quinidine in concentrations
that exert little effect on normal Purkinje tissue, 1 to 2 micrograms/ml,
greatly impaired conduction and markedly prolonged refractoriness across
the ischemic gap. The drug effected these changes by (1) extending the
inexcitable zone within the depressed region, (2) decreasing the amplitude
of the input signal entering this zone, and (3) decreasing the excitability
of the tissue beyond the depressed zone (evaluated by current clamp
techniques). These actions of the drug produced both antiarrhythmic and
proarrhythmic effects. When the initial level of conduction impairment was
high, quinidine totally suppressed reflected reentry at all frequencies by
precipitating complete anterograde conduction block. At intermediate levels
of block, the drug generally caused a prominent shift of the frequency
dependence of reentrant activity to lower stimulation rates. Finally, when
conduction was relatively less impaired, quinidine created the conditions
for reflected reentry to occur. Our results suggest that the heart rate
dependence of reentrant arrhythmias might be of prognostic value in the
administration of antiarrhythmic drugs.
ARTICLES
Mechanisms underlying the antiarrhythmic and arrhythmogenic actions of quinidine in a Purkinje fiber-ischemic gap preparation of reflected reentry
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