Transmembrane potential changes caused by shocks in guinea pig
papillary muscle.
Zhou, Xiaohong, William M Smith, Dennis L. Rollins, Raymond E Ideker.
Departments of Medicine and Pathology, Duke University Medical
Center, Durham, North Carolina, 27710, the Engineering Research
Center in Emerging Cardiovascular Technologies, School of
Engineering, Duke University, Durham, North Carolina, 27706 and the
Division of Cardiovascular Disease, Department of Medicine,
University of Alabama at Birmingham, Birmingham, Alabama 35294
APStracts 3:0198H, 1996.
To study the transmembrane potential changes (_V[mu]) caused by
extracellular field stimulation, V[mu] was recorded in 10 guinea pig
papillary muscles by a double-barrel microelectrode which could
eliminate the shock artifact during the V[mu] recording. Following 20
S1 stimuli at twice diastolic threshold, a 10 msec S2 shock field was
delivered through shock electrodes 2 cm on either side of the tissue
during the action potential plateau with a 30 msec S1-S2 interval or
during diastole. Six shock strengths were given which created field
strengths of 1.8+/-0.4, 3.8+/-0.7, 5.6+/-0.9, 7.2+/-1.1, 11.1+/-1.9
and 17.8+/-1.5 V/cm at the papillary muscle. Shocks of both
polarities were given. The tissue was then treated with either 30
[mu]M TTX (n=5) or 30 [mu]M TTX plus Ca++-free (n=5) perfusion. The
above six shock strengths with both polarities were given again
during diastole. Results: For shocks during the action potential
plateau, the net magnitudes of the _V[mu] caused by the above six
potential gradients were 22.4+/-9.6, 43.6+/-17.4, 54.7+/-17.9,
60.4+/-18.1, 65.4+/-13.7 and 66.4+/-12.2 mV (p<.01 among changes
caused by six shock strengths) for shocks causing depolarization and
41.1+/-16.5, 68.3+/-22, 80.5+/-20.4, 84.0+/-19.5, 93.6+/-16.3 and
98.9+/-15.4 mV (p<.01 among changes caused by six shock
strengths) for shocks causing hyperpolarization. Though _V[mu]
increased as the shock potential gradient increased, the relationship
was not linear. For shocks during diastole, hyperpolarizing shocks
induced triphasic changes in V[mu] during the shock, i.e., initial
hyperpolarization, then depolarization, followed again by
hyperpolarization. A new depolarization upstroke occurred immediately
after the end of the shock. After TTX or TTX plus Ca++-free
perfusion, neither twice nor 10 times diastolic threshold S1 could
induce an action potential, but a shock field of 1.8+/-0.2 V/cm still
induced action potentials. The peak value of depolarization measured
with respect to the resting potential (-87+/-5 mV) during the
hyperpolarizing shock decreased from +14+/-22 mV before TTX perfusion
to -66+/-30 mV with TTX perfusion (p<0.01). The fast upstroke
rate of depolarization both during and immediately after the end of
hyperpolarizing shocks was inhibited by TTX perfusion. Conclusion:
(1) the relationship between the _V[mu] and the shock potential
gradient is not linear; (2) field but not point stimulation can
induce an action potential when sodium channels are inactivated; and
(3) during diastole sodium channels responsible for fast
depolarization are activated twice by a 10 msec hyperpolarizing
shock, once during shock-induced hyperpolarization and again
immediately after the end of the shock.
Received 6 October 1995; accepted in final form 24 April 1996.
APS Manuscript Number H943-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 8 May 96