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Gen. Pharmac. Vol. 21, No.5, pp. 747-751, 1990
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USE-DEPENDENT ACTION OF ANTIARRHYTHMIC
DRUGS IN FROG SKELETAL MUSCLE AND CANINE
CARDIAC PURKINJE FIBER
PETER P. NANASI,* ANDRAS VARR6,
1
DAVID A. LATHROP
1
and MIKLOS DANK6
Department of Physiology, University Medical School of Debrecen, P.O. Box 22, H-4012 Debrecen,
Hungary and
1
Department of Pediatrics, University of Cincinnati College of Medicine, Eiland and
Bethesda Ave., Cincinnati, OH 45229, U.S.A.
(Received 2 January 1990)
Abstract---!. Conventional microelectrode techniques were used to study the effect of quinidine (10
lidocaine (20 and verapamil (3-10 ,uM) on action potential upstroke (V::;,.) in frog skeletal muscle
and dog Purkinje fiber.
2. The frequency-dependent nature of v:., depression induced by these drugs was similar in both
preparations, however, quinidine was more potent in skeletal muscle while lidocaine was in Purkinje fibers.
3. In skeletal muscle tetrodotoxin (3 and 15 nM) and low concentrations of antiarrhythmic drugs
proportionally reduced the maximum velocity of depolarization and repolarization (V: .. and V,;;.,,
respectively), whereas v.;; .. was more depressed than .. by high concentrations (50-200 of
antiarrhythmics. Decreases in the overshoot potential were proportional to the .. block in the case of
each drug.
4. These results indicate that therapeutically relevant concentrations of quinidine and lidocaine inhibit
skeletal muscle Na+ channels in a use-dependent manner similar to heart, while at higher concentrations
the K + channels may also be blocked. Therapeutic implications of the results are: discussed.
INTRODliCTION
It is well known that class I antiarrhythmic agents
(Vaughan Williams, 1975) depress excitability, maxi-
mum upstroke velocity (V!..) and conduction
in cardiac tissues in a use-dependent manner
(Hondeghem and Katzung, 1984; Campbell, 1983;
Grant et al., 1984) which is believed to play an
important role in their therapeutic action. Although
the effects of these drugs on the fast Na + current or
the •• were studied extensively in different cardiac
preparations (Courtney, 1980; Grant et a!., 1984;
Campbell, 1983; Varr6 et al., 1985) there are only few
data available in skeletal muscle with therapeutically
relevant concentrations (Andersson, 1973; Harvey
and Rang, 1974). In addition, considerable differ-
ences between cardiac and skeletal muscle have been
reported in respect of sensitivity and mode of action
of tetrodotoxin (TTX) (Jaimovich et a/., 1976;
Clarkson eta/., 1988) indicating that the Na + chan-
nels in these preparations are not fully identical.
However, Courtney (1981) did not observe substan-
tial differences between guinea-pig cardiac and frog
skeletal muscle on fast Na + current with lidocaine,
mexiletine and tocainide. In our previous work
(Nanasi et a!., 1987) we studied the effect of bency-
clane on v;;; •• in dog cardiac Purkinjc fibers and frog
skeletal muscle. Both the magnitude and the use-
dependent nature of the bencyclane-induced v;;; ••
block were comparable. In the present report we
*To whom correspondence should be addressed: Dr Peter P.
Namisi, Children's Hospital Research Foundation,
Division of Cardiology, Eiland and Bethesda Avenues,
Cincinnati, OH 45229, U.S.A.
747
compared the effects of therapeutic concentrations of
quinidine and lidocaine, and high concentrations of
verapamil on V •• in frog skeletal muscle and canine
Purkinje strands. It was found, that the use-depen-
dent depression of v;;;., induced by the studied
antiarrhythmic drugs was similar in the two different
preparations, therefore, changes in the function of
skeletal muscles may be anticipated during the thera-
peutic application of these agents.
METHODS
Electrophysiological measurements in frog skeletal muscle
The experiments were performed in superficial fibers of
frog sartorius muscle (Rana esculenta) at room temperature
in Ringer's solution (Na +, 120.2; K + 2.5; Ca2+ 1.8; CI-
121.1; HPOl- 2.15; H
2
P04 0.85 mM) buffered at
pH 7.0 ± 0.05. Two glass microelectrodcs, filled with 2.5 M
KCI, were inserted into the same fiber for the purpose of
stimulation and recording. Transmembrane potential
changes and their first time derivatives, obtained using an
analogue dilferentiator, were monitored on a dual beam
digital storage oscilloscope (Gould OS-4000) and displayed
on a chart recorder (Servogor 460) for later analysis. Trains
of electrical stimuli (I in amplitude and 0.5 msec in
duration for each pulse) were delivered through the current
passing microclectrode. The train durations were 45 msec
and 10 sec for trains of 100 and 4Hz frequency, respectively.
In both cases, the use-dependent reduction of V ;:;., was
calculated using the following formula:
v+ ·v·
y = la0_!!'ta.X 1st (Drug) , I OO
V last/ V 1st (Control)
(I)
and the term of (I 00- Y) gave the measure of block as
percentage. Changes in the maximum velocity of repolariz-
ation (V,;;.,) were calculated in the same way, while changes
in the overshoot potential (OSP) were given as differences