INTRODUCTION: The purpose of this investigation was to study the transmembrane potential changes (delta Vm) during extracellular electrical field stimulation. METHODS AND RESULTS: Vm was recorded in seven guinea pig papillary muscles in a tissue bath by a double-barrel microelectrode with one barrel in and the other just outside a cell while shocks were given across the bath. The short distance (15 to 30 microns) between the two microelectrode tips and alignment of the tips parallel to the shock electrodes eliminated the shock artifact. Following ten S1 stimuli, an S2 shock field created by a 10-msec square wave was delivered during the action potential plateau or during diastole through shock electrodes 1 cm on either side of the tissue. Four shock strengths creating field strengths of 1.7 +/- 0.1, 2.9 +/- 0.2, 6.1 +/- 0.6, and 8.8 +/- 0.9 V/cm were given for the same impalement. Both shock polarities were given at each shock strength. For shocks delivered during the action potential plateau, the magnitudes of the peak delta Vm caused by the above four potential gradients were 21.1 +/- 8.2, 33.6 +/- 13.6, 49.9 +/- 24.2, and 52.3 +/- 28.0 mV (P < 0.05 among the four groups) for the shocks causing depolarization and 37.9 +/- 14.2, 56.6 +/- 16.4, 83.1 +/- 19.4, and 92.9 +/- 29.1 mV (P < 0.05 among the four groups) for the shocks causing hyperpolarization. Though delta Vm increased as potential gradients increased, the relationship was not linear. The magnitude of hyperpolarization was 1.9 +/- 0.5 times that of depolarization when the shock polarity was reversed (P < 0.05). As potential gradients increased from 1.7 +/- 0.1 to 8.8 +/- 0.9 V/cm, the time constant of the membrane response decreased significantly from 3.5 +/- 1.8 to 1.6 +/- 0.7 msec for depolarizing shocks and from 6.0 +/- 3.1 to 3.4 +/- 1.9 msec for hyperpolarizing shocks (P < 0.01 vs depolarizing shocks). For shocks delivered during diastole, hyperpolarizing shocks induced triphasic changes in Vm during the shock, i.e., initial hyperpolarization, than depolarization, followed again by hyperpolarization. CONCLUSION: During the action potential plateau, the membrane response cannot be represented by a classic passive RC membrane model. During diastole, activation upstrokes occur even during hyperpolarization caused by shocks creating potential gradients between approximately 2 and 9 V/cm.
INTRODUCTION: The purpose of this investigation was to study the transmembrane potential changes (delta Vm) during extracellular electrical field stimulation. METHODS AND RESULTS: Vm was recorded in seven guinea pig papillary muscles in a tissue bath by a double-barrel microelectrode with one barrel in and the other just outside a cell while shocks were given across the bath. The short distance (15 to 30 microns) between the two microelectrode tips and alignment of the tips parallel to the shock electrodes eliminated the shock artifact. Following ten S1 stimuli, an S2 shock field created by a 10-msec square wave was delivered during the action potential plateau or during diastole through shock electrodes 1 cm on either side of the tissue. Four shock strengths creating field strengths of 1.7 +/- 0.1, 2.9 +/- 0.2, 6.1 +/- 0.6, and 8.8 +/- 0.9 V/cm were given for the same impalement. Both shock polarities were given at each shock strength. For shocks delivered during the action potential plateau, the magnitudes of the peak delta Vm caused by the above four potential gradients were 21.1 +/- 8.2, 33.6 +/- 13.6, 49.9 +/- 24.2, and 52.3 +/- 28.0 mV (P < 0.05 among the four groups) for the shocks causing depolarization and 37.9 +/- 14.2, 56.6 +/- 16.4, 83.1 +/- 19.4, and 92.9 +/- 29.1 mV (P < 0.05 among the four groups) for the shocks causing hyperpolarization. Though delta Vm increased as potential gradients increased, the relationship was not linear. The magnitude of hyperpolarization was 1.9 +/- 0.5 times that of depolarization when the shock polarity was reversed (P < 0.05). As potential gradients increased from 1.7 +/- 0.1 to 8.8 +/- 0.9 V/cm, the time constant of the membrane response decreased significantly from 3.5 +/- 1.8 to 1.6 +/- 0.7 msec for depolarizing shocks and from 6.0 +/- 3.1 to 3.4 +/- 1.9 msec for hyperpolarizing shocks (P < 0.01 vs depolarizing shocks). For shocks delivered during diastole, hyperpolarizing shocks induced triphasic changes in Vm during the shock, i.e., initial hyperpolarization, than depolarization, followed again by hyperpolarization. CONCLUSION: During the action potential plateau, the membrane response cannot be represented by a classic passive RC membrane model. During diastole, activation upstrokes occur even during hyperpolarization caused by shocks creating potential gradients between approximately 2 and 9 V/cm.
Authors: M M Maleckar; M C Woods; V Y Sidorov; M R Holcomb; D N Mashburn; J P Wikswo; N A Trayanova Journal: Am J Physiol Heart Circ Physiol Date: 2008-08-15 Impact factor: 4.733