The electrophysiological effects of disopyramide phosphate on canine ventricular muscle and Purkinfe fibers in normal and low potassium

1978 ◽  
Vol 56 (1) ◽  
pp. 139-149 ◽  
Author(s):  
Teresa Kus ◽  
Betty I. Sasyniuk
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Time Course ◽  
Antiarrhythmic Effect ◽  
Extracellular Potassium ◽  
Ventricular Muscle ◽  
Extracellular Potassium Concentration ◽  
Course Of Action ◽  
Low K ◽  
Electrophysiological Effects

We studied the effect of lowering the extracellular potassium concentration ([K+]0) on the electrophysiological actions of disopyramide phosphate, a new antiarrhythmic drug. At low [K+]0, therapeutic concentrations of disopyramide phosphate caused significantly less depression of action potential amplitude and maximum upstroke velocity of both Purkinje fiber and ventricular muscle action potentials. The drug shifted the membrane responsiveness curve along the voltage axis to more negative membrane potentials regardless of [K+]0. However, a greater shift occurred when [K+]0 was normal. Disopyramide phosphate prolonged both action potential duration and effective refractory period in all fibers but there was consistently greater prolongation of these parameters at low [K+]0, More importantly, disopyramide phosphate altered repolarization time course of action potentials in such a way that action potentials with dissimilar durations throughout the ventricular conducting system became more equal. The drug was less effective in decreasing this disparity in action potential durations throughout the ventricles in the presence of low [K+]0. These modifications of the electrophysiological actions of disopyramide by low [K+]0 suggest that a therapeutic concentration of disopyramide might have less of an antiarrhythmic effect in the presence of hypokalemia.

scholarly journals Junctional resistance and action potential delay between embryonic heart cell aggregates.

1980 ◽  
Vol 75 (6) ◽  
pp. 633-654 ◽  
Author(s):  
D E Clapham ◽  
A Shrier ◽  
R L DeHaan
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Time Course ◽  
Potassium Concentration ◽  
Aggregate Size ◽  
Heart Cell ◽  
Extracellular Potassium ◽  
Cell Aggregates ◽  
Extracellular Potassium Concentration ◽  
Junctional Resistance

Spheroidal aggregates of embryonic chick ventricle cells were brought into contact and allowed to synchronize their spontaneous beats. Action potentials were recorded with both intracellular and extracellular electrodes. The degree of electrical interaction between the newly apposed aggregates was assessed by measuring the delay or latency (L) between the entrained action potentials, and by determining directly interaggregate coupling resistance (Rc) with injected current pulses. Aggregate size, contact area between the aggregates, and extracellular potassium concentration (Ko+) were important variables regulating the time-course of coupling. When these variables were controlled, L and Rc were found to be linearly related after beat synchrony was achieved. In 4.8 mM Ko+ L/Rc = 3.7 ms/M omega; in 1.3 mM Ko+ L/Rc = 10.1 ms/M omega. We conclude that action potential delay between heart cell aggregates can be related quantitatively to Rc.

Effect of Several Cations on Transmembrane Potentials of Cardiac Muscle

1956 ◽  
Vol 186 (2) ◽  
pp. 317-324 ◽  
Author(s):  
Brian F. Hoffman ◽  
E. E. Suckling
Keyword(s):  
Action Potential ◽  
Cardiac Muscle ◽  
Action Potentials ◽  
Time Course ◽  
Pacemaker Activity ◽  
Transmembrane Potentials ◽  
High K ◽  
Intracellular Microelectrodes ◽  
Simultaneous Decrease ◽  
Low K

The effects of changes in the extracellular concentrations of Ca, K and Mg on the transmembrane resting and action potentials of single fibers of the auricle, ventricle and specialized conducting system of the dog heart have been studied by means of intracellular microelectrodes. With respect to Ca, the three tissues exhibit quite different sensitivities. Changes in concentration of this ion alter the time course of the action potential recorded from auricle and ventricle but have little effect on the action potential configuration of the Purkinje fiber. In the latter tissue, on the other hand, pacemaker activity is most strongly enhanced by Ca depletion and excitability is lost at Ca concentrations permitting normal propagation in papillary muscle. The effect of K on the resting transmembrane potential is dependent on the simultaneous Ca concentration. The interrelationship is such that the depolarizing effect of high K is decreased by elevated Ca and the depolarization produced by low K is diminished by low levels of Ca. Changes in the concentration of Mg have little effect on the transmembrane potentials of cardiac muscle unless the level of Ca is low. Under this condition a simultaneous decrease in Mg gives rise to a marked prolongation of the action potential duration of both auricle and ventricle. Some evidence for the basic similarity of the processes underlying repolarization in these three tissues is presented and it is thought the normally encountered differences in their action potentials may be related to the sensitivity of each tissue to extracellular Ca.

scholarly journals Positive and Negative Inotropic Effects of Elevated Extracellular Potassium Level on Mammalian Ventricular Muscle

1972 ◽  
Vol 60 (3) ◽  
pp. 351-365 ◽  
Author(s):  
Frederic Kavaler ◽  
Paul M. Hyman ◽  
Robert B. Lefkowitz
Keyword(s):  
Steady State ◽  
Action Potential ◽  
Time Course ◽  
Potassium Level ◽  
Positive Inotropic Effect ◽  
Potassium Concentration ◽  
Inotropic Effect ◽  
Extracellular Potassium ◽  
Ventricular Muscle ◽  
Inotropic Effects

The effect of moderate elevation in extracellular potassium concentration (up to 12 mM) on contraction of cat ventricular muscle was examined. Isometric force development was recorded from eight excised trabeculae and from six coronary-perfused in situ papillary muscle preparations. Contraction in the steady state was variably affected, sometimes decreasing monotonically, sometimes remaining unchanged, with increasing potassium level. In 11 of these 14 preparations, the steady state was preceded by a transient period in which the contraction was augmented. In addition, eight excised trabeculae were used in an experimental arrangement designed to distinguish between inotropic effects caused by potassium-induced alterations in the action potential and other, more direct, effects of this ion on contraction. The negative inotropic effect is attributable to a potassium-induced reduction in the amplitude and/or duration of the action potential plateau. The positive inotropic effect was found in experimental arrangements where effects of the potassium-rich medium on action potential time-course were effectively "buffered." The positive inotropic effect thus depends on the presence of the elevated potassium concentration and can occur independently of effects on the action potential time-course.

Calcium Dynamics and Compartmentalization in Leech Neurons

2005 ◽  
Vol 94 (6) ◽  
pp. 4430-4440 ◽  
Author(s):  
Sofija Andjelic ◽  
Vincent Torre
Keyword(s):  
Information Processing ◽  
Action Potential ◽  
Action Potentials ◽  
Time Course ◽  
Ccd Camera ◽  
Calcium Dynamics ◽  
Single Action ◽  
Single Action Potential ◽  
Calcium Indicator ◽  
Mechanosensory Neurons

Calcium dynamics in leech neurons were studied using a fast CCD camera. Fluorescence changes (Δ F/ F) of the membrane impermeable calcium indicator Oregon Green were measured. The dye was pressure injected into the soma of neurons under investigation. Δ F/ F caused by a single action potential (AP) in mechanosensory neurons had approximately the same amplitude and time course in the soma and in distal processes. By contrast, in other neurons such as the Anterior Pagoda neuron, the Annulus Erector motoneuron, the L motoneuron, and other motoneurons, APs evoked by passing depolarizing current in the soma produced much larger fluorescence changes in distal processes than in the soma. When APs were evoked by stimulating one distal axon through the root, Δ F/ F was large in all distal processes but very small in the soma. Our results show a clear compartmentalization of calcium dynamics in most leech neurons in which the soma does not give propagating action potentials. In such cells, the soma, while not excitable, can affect information processing by modulating the sites of origin and conduction of AP propagation in distal excitable processes.

Effects of estrogen on action potential and membrane currents in guinea pig ventricular myocytes

1999 ◽  
Vol 277 (2) ◽  
pp. H826-H833 ◽  
Author(s):  
Seiko Tanabe ◽  
Toshio Hata ◽  
Masayasu Hiraoka
Keyword(s):  
Guinea Pig ◽  
Action Potential ◽  
Action Potentials ◽  
Voltage Dependence ◽  
Ventricular Myocytes ◽  
Membrane Currents ◽  
Patch Clamp Technique ◽  
17Β Estradiol ◽  
Electrophysiological Effects ◽  
Ionic Basis

To explore a possible ionic basis for the prolonged Q-T interval in women compared with that in men, we investigated the electrophysiological effects of estrogen in isolated guinea pig ventricular myocytes. Action potentials and membrane currents were recorded using the whole cell configuration of the patch-clamp technique. Application of 17β-estradiol (10–30 μM) significantly prolonged the action potential duration (APD) at 20% (APD20) and 90% repolarization (APD90) at stimulation rates of 0.1–2.0 Hz. In the presence of 30 μM 17β-estradiol, APD20 and APD90 at 0.1 Hz were prolonged by 46.2 ± 17.1 and 63.4 ± 11.7% of the control ( n = 5), respectively. In the presence of 30 μM 17β-estradiol the peak inward Ca2+ current ( I CaL) was decreased to 80.1 ± 2.5% of the control ( n = 4) without a shift in its voltage dependence. Application of 30 μM 17β-estradiol decreased the rapidly activating component of the delayed outward K+ current ( I Kr) to 63.4 ± 8% and the slowly activating component ( I Ks) to 65.8 ± 8.7% with respect to the control; the inward rectifier K+ current was barely affected. The results suggest that 17β-estradiol prolonged APD mainly by inhibiting the I Kcomponents I Krand I Ks.

Excitability and electrical response of ischemic heart muscle

1960 ◽  
Vol 198 (6) ◽  
pp. 1143-1147 ◽  
Author(s):  
Chandler McC. Brooks ◽  
Jerome L. Gilbert ◽  
Martin E. Greenspan ◽  
Gertrude Lange ◽  
Hector M. Mazzella
Keyword(s):  
Action Potential ◽  
Blood Supply ◽  
Heart Muscle ◽  
Action Potentials ◽  
Electrical Response ◽  
Left Ventricular ◽  
Ischemic Heart ◽  
Monophasic Action Potential ◽  
Ventricular Muscle ◽  
Refractory Periods

Measurements were made of the changes in the monophasic action potential, excitability, durations of the refractory periods and conduction times in an area of left ventricular muscle during the development of ischemia subsequent to ligation of the ramus descendens anterior. The degree and duration of the ischemia produced varied greatly and effects were related thereto. It was found that action potentials shortened as did the refractory periods; thresholds fell momentarily and then rose progressively as tissue responsiveness failed due to continuing ischemia. Latency of responses increased, the action potentials decreased in amplitude and alternation occurred before the tissue became completely unresponsive. Early re-establishment of a blood supply caused a reversal of the abnormalities. The significance of these changes to the origin of arrhythmias is discussed.

Time course of postnatal changes in rat heart action potential and in transient outward current is different

1994 ◽  
Vol 267 (3) ◽  
pp. H1157-H1166 ◽  
Author(s):  
G. M. Wahler ◽  
S. J. Dollinger ◽  
J. M. Smith ◽  
K. L. Flemal
Keyword(s):  
Action Potential ◽  
Rat Heart ◽  
Action Potentials ◽  
Time Course ◽  
Outward Current ◽  
Transient Outward Current ◽  
Papillary Muscles ◽  
Isolated Cells ◽  
Time Courses ◽  
Action Potential Shortening

The rat ventricular action potential shortens after birth. The contribution of increases in the transient outward current (Ito) to postnatal action potential shortening was assessed by measuring Ito in isolated cells and by determining the effect of 2 mM 4-aminopyridine (4-AP) on the action potentials of papillary muscles. 4-AP had no effect on 1-day action potential duration at 25% repolarization (APD25), and 1-day cells had little Ito. In 8- to 10-day muscles, 4-AP caused a small, but significant, increase in APD25. Ito increased slightly between day 1 and days 8-10, but this increase was not significant. Most of the increase in Ito (79%) and in the response to 4-AP (64%) occurred between days 8-10 and adult; however, approximately 75% of the APD25 shortening took place by days 8-10. Thus, while Ito may contribute to repolarization in late neonatal and adult cells, the different time courses of action potential shortening and increases in Ito suggest that changes in Ito are unlikely to be responsible for most of the postnatal action potential shortening.

Correlation of light-induced changes in retinal extracellular potassium concentration with c-wave of the electroretinogram

1976 ◽  
Vol 39 (5) ◽  
pp. 1117-1133 ◽  
Author(s):  
B. Oakley ◽  
D. G. Green
Keyword(s):  
Time Course ◽  
Potassium Concentration ◽  
Action Spectrum ◽  
Extracellular Potassium ◽  
Threshold Curve ◽  
Photoreceptor Layer ◽  
Extracellular Potassium Concentration ◽  
Increment Threshold ◽  
Induced Changes ◽  
Pigment Epithelial Cells

1. Double-barrel, potassium-specific microelectrodes have been used to measure light-induced transient changes in [K+]o in the frog eye cup preparation. These changes in [K+]o have been termed the potassioretinogram (KRG). 2. The KRG consists of two components: a rapid increase in [K+]o in the proximal retina and a slow decrease in [K+]o in the distal retina. 3. The KRG decrease has the rhodopsin action spectrum, is maximal in the photoreceptor layer, persists after aspartate treatment, and has an increment threshold curve which saturates at moderate background intensities. The rhodopsin rods are, therefore, most likely the only neurons which generate this ionic change, although the Muller (glial) cells may also be involved in this process. 4. The KRG decrease has the same time course as the c-wave of the electroretinogram for all variations in the stimulus parameters, including intensity, duration, and chromaticity. 5. It is suggested that the c-wave may be produced by the pigment epithelial cells as they hyperpolarize in response to the decrease in [K+]o around the photoreceptors.

scholarly journals Spreading Depression Can Be Elicited in Brain Stem of Immature But Not Adult Rats

2003 ◽  
Vol 90 (4) ◽  
pp. 2163-2170 ◽  
Author(s):  
Frank Richter ◽  
Sven Rupprecht ◽  
Alfred Lehmenkühler ◽  
Hans-Georg Schaible
Keyword(s):  
Brain Stem ◽  
Time Course ◽  
Spreading Depression ◽  
Chloride Ions ◽  
Extracellular Potassium ◽  
Peak Time ◽  
Adult Rats ◽  
Extracellular Potassium Concentration ◽  
Nmda Receptor Blocker ◽  
The Brain

Spreading depression (SD), a neuronal mechanism involved in brain pathophysiology, occurs in brain areas with high neuronal density such as the cerebral cortex. By contrast, the brain stem is thought to be resistant to SD. Here we show that DC shifts resembling cortical SD can be elicited in rat brain stem by topical application of KCl but not by pricking the brain stem. However, this was only possible until postnatal day 13, and, in addition, susceptibility for SD had to be enhanced. The latter was achieved by superfusion of the brain stem for 45 min with a solution containing acetate instead of chloride ions. Transient asphyxia or hypoxia by 2 min breathing 6% O2 in N2 had a similar effect. Negative brain stem DC deflections were paralleled by an increase of extracellular potassium concentration ≤40 mM and were spreading, but unlike cortical SD they were not inducible by glutamate and N-methyl-d-aspartate (NMDA). Time course and slope of brain stem SD either resembled cortical SD or were long-lasting and sustained. The latter stopped normal breathing. Different from cortical SD, negative brain stem DC deflections were changed in their slope (mostly converted into sustained shape, peak time was significantly prolonged, decline-time and duration were prolonged), but not abolished by the NMDA receptor blocker MK-801. Thus we demonstrate that the immature brain stem has the capacity to generate negative DC shifts, which could be relevant as a risk factor in newborn brain stem function.

Posttetanic hyperpolarization produced by electrogenic Na(+)-K+ pump in lizard axons impaled near their motor terminals

1993 ◽  
Vol 70 (5) ◽  
pp. 1874-1884 ◽  
Author(s):  
K. Morita ◽  
G. David ◽  
J. N. Barrett ◽  
E. F. Barrett
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Time Course ◽  
Input Resistance ◽  
Peak Amplitude ◽  
Resting Potential ◽  
Tetanic Stimulation ◽  
Train Duration ◽  
Consistent Change ◽  
Nodal Voltage

1. The hyperpolarization that follows tetanic stimulation was recorded intra-axonally from the internodal region of intramuscular myelinated motor axons. 2. The peak amplitude of the posttetanic hyperpolarization (PTH) that followed stimulation at 20-100 Hz for < or = 35 s increased with increasing train duration, reaching a maximum of 22 mV. PTH decayed over a time course that increased from tens to hundreds of seconds with increasing train duration. For a given frequency of stimulation the time integral of PTH was proportional to the number of stimuli in the train, averaging 3-4 mV.s per action potential. 3. Ouabain (0.1-1 mM) and cyanide (1 mM) depolarized the resting potential and abolished PTH. Tetanic stimulation in ouabain was followed by a slowly decaying depolarization (probably due to extra-axonal K+ accumulation) whose magnitude and duration increased as the duration of the train increased. 4. Axonal input resistance showed no consistent change during PTH in normal solution but increased during PTH in the presence of 3 mM Cs+ (which blocks axonal inward rectifier currents). 5. PTH was abolished when bath Na+ was replaced by Li+ or choline. PTH persisted after removal of bath Ca2+ and addition of 2 mM Mn2+. 6. Removal of bath K+ abolished the PTH recorded after brief stimulus trains and greatly reduced the duration of PTH recorded after longer stimulus trains. 7. A brief application of 10 mM K+, which normally depolarizes axons, produced a ouabain-sensitive hyperpolarization in axons bathed in K(+)-free solution. 8. These observations suggest that in these myelinated axons PTH is produced mainly by activation of an electrogenic Na(+)-K(+)-ATPase, rather than by changes in K+ permeability or transmembrane [K+] gradients. This conclusion is supported by calculations showing agreement between estimates of Na+ efflux/impulse based on PTH measurements and estimates of Na+ influx/impulse based on nodal voltage-clamp measurements. Pump activity also appears to contribute to the resting potential. 9. The stimulus intensity required to initiate a propagating action potential increased during PTH but decreased during the posttetanic depolarization recorded in ouabain. Thus changes in axonal excitability after tetanic stimulation correlate with changes in the posttetanic membrane potential. 10. Action potentials that propagated during PTH had a larger peak amplitude and were followed by a larger and longer depolarizing afterpotential than action potentials elicited at the resting potential. This enhancement of the depolarizing afterpotential is consistent with previous reports of an increased superexcitable period after action potentials evoked during PTH.

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