scholarly journals The relationship among intracellular sodium activity, calcium, and strophanthidin inotropy in canine cardiac Purkinje fibers.

1984 ◽  
Vol 83 (2) ◽  
pp. 287-307 ◽  
Author(s):  
M Vassalle ◽  
C O Lee
Keyword(s):  
Action Potential ◽  
Calcium Influx ◽  
Intracellular Sodium ◽  
Sodium Ion ◽  
Inotropic Effect ◽  
Similar Time ◽  
Tension Development ◽  
Purkinje Fibers ◽  
Cardiac Purkinje Fibers ◽  
High Calcium

The role of sodium and calcium ions in strophanthidin inotropy was studied by measuring simultaneously the electrical, mechanical, and intracellular sodium ion activities in electrically driven cardiac Purkinje fibers under conditions that change the intracellular sodium or calcium level (tetrodotoxin, strophanthidin, high calcium, and norepinephrine). Tetrodotoxin (TTX; 1-5 X 10(-6)M) shifted the action potential plateau to more negative values, shortened the action potential duration, and decreased the contractile tension and the intracellular sodium ion activity (aiNa). The changes in tension and in aiNa caused by TTX appear to be related since they had similar time courses. Strophanthidin (2-5 X 10(-7)M) increased tension and aiNa less in the presence of TTX, and, for any given value of aiNa, tension was less than in the absence of TTX. Increasing extracellular calcium (from 1.8 to 3.3-3.6 mM) or adding norepinephrine (0.5-1 X 10(-6)M) increased tension and decreased aiNa less in the presence than in the absence of TTX. When two of the above procedures were combined, the results were different. Thus, during the increase in aiNa and tension caused by strophanthidin in the presence of TTX, increasing calcium or adding norepinephrine increased tension markedly but did not increase aiNa further. In a TTX-high calcium or TTX-norepinephrine solution, adding strophanthidin increased both tension and aiNa, and the increase in tension was far greater than in the presence of TTX alone. The results indicate that: (a) the contractile force in Purkinje fibers is affected by a change in aiNa; (b) a decrease in aiNa by TTX markedly reduces the inotropic effect of strophanthidin, possibly as a consequence of depletion of intracellular calcium; (c) increasing calcium influx with norepinephrine or high calcium in the TTX-strophanthidin solution produces a potentiation of tension development, even if aiNa does not increase further; and (d) when the calcium influx is already increased by high calcium or norepinephrine, strophanthidin has its usual inotropic effect even in the presence of TTX. In conclusion, the positive inotropic effect of strophanthidin requires that an increase in aiNa be associated with suitable calcium availability.

Modulation of intracellular Na+ activity and cardiac force by norepinephrine and Ca2+

1983 ◽  
Vol 244 (1) ◽  
pp. C110-C114 ◽  
Author(s):  
C. O. Lee ◽  
M. Vassalle
Keyword(s):  
Contractile Force ◽  
Intracellular Sodium ◽  
Sodium Ion ◽  
Purkinje Fibers ◽  
Intracellular Na Activity ◽  
Cardiac Purkinje Fibers ◽  
High Calcium ◽  
Ion Activity ◽  
Ion Activities ◽  
Stimulation Of

The actions of norepinephrine and high calcium on the electrical, mechanical, and intracellular sodium ion activities were studied in electrically driven canine cardiac Purkinje fibers under different conditions. It was found that norepinephrine and high calcium decrease intracellular sodium ion activity (aiNa). The exposure to either agent is followed by a transient decline of force that correlates with the lower aiNa. Inhibition of the Na+ -K+ pump by strophanthidin reduces or abolishes the decrease in aiNa by norepinephrine but not that by high calcium. It is concluded that norepinephrine and high calcium both decrease aiNa and thereby the contractile force but (unlike high calcium) norepinephrine acts through the stimulation of the Na+ -K+ pump.

Role of calcium and sodium in strophanthidin inotropy in cardiac Purkinje fibers

1981 ◽  
Vol 240 (4) ◽  
pp. H561-H570
Author(s):  
M. L. Bhattacharyya ◽  
M. Vassalle
Keyword(s):  
Inotropic Effect ◽  
Force Of Contraction ◽  
Tyrode Solution ◽  
Purkinje Fibers ◽  
Low Concentration ◽  
Cellular Calcium ◽  
Cardiac Purkinje Fibers ◽  
High Calcium

The effects of strophanthidin on electrical and mechanical events in canine cardiac Purkinje fibers were studied in vitro in the absence and presence of tetrodotoxin (TTX), norepinephrine, and high calcium. In Tyrode solution, strophanthidin (1-3 X 10(-7) M), norepinephrine (3-5 X 10(-7) M), and high calcium 8.1 mM) increased the force of contraction, and TTX markedly reduced it. In the presence of TTX, strophanthidin had little or no inotropic effect, whereas that of norepinephrine and high calcium was less than in Tyrode solution. In the presence of TTX, strophanthidin increased force markedly if (and as long as) either norepinephrine or high calcium were also present. A higher dose of strophanthidin (10(-6) M) induced a markedly delayed increase in force in presence of TTX. The results suggest that, in the presence of TTX, in a low concentration strophanthidin has little effect on force, because cellular calcium is low; however, it becomes effective when the calcium is increased by norepinephrine or high calcium. In toxic doses, strophanthidin increases force even in the presence of TTX as the inhibition of the pump should increase intracellular sodium and therefore calcium.

Intracellular sodium ion activity: reliable measurement and stimulation-induced change in cardiac Purkinje fibers

1987 ◽  
Vol 65 (5) ◽  
pp. 954-962 ◽  
Author(s):  
Chin O. Lee ◽  
Wook B. Im ◽  
Jong K. Sonn
Keyword(s):  
Membrane Potential ◽  
Time Constant ◽  
Fast Response ◽  
Intracellular Sodium ◽  
Sodium Ion ◽  
Sodium Influx ◽  
Stimulation Rate ◽  
Purkinje Fibers ◽  
Cardiac Purkinje Fibers ◽  
Ion Activity

Recently Na+-selective microelectrodes (NaSM) have been used to measure quantitatively small changes in intracellular sodium ion activity [Formula: see text] and to determine a precise time course of comparatively rapid change in [Formula: see text]. In such studies, accurate measurement of [Formula: see text] requires the following criteria: (i) NaSM should have a fast response time and (ii) an NaSM and a conventional voltage microelectrode should measure the same membrane potential. These criteria were evaluated by measuring [Formula: see text] when membrane potential of cardiac Purkinje fibers was suddenly hyperpolarized and depolarized by changing stimulation rate. The NaSM coated with a conductive silver paint had fast response times so that rapid changes in [Formula: see text] could be reliably measured. The cardiac Purkinje fibers stimulated at a constant rate generated uniform membrane voltage and the NaSM and conventional microelectrode measured virtually the same membrane potential. This result is somewhat different from that reported under voltage-clamp condition by other investigators. The [Formula: see text] of the fibers increased as the stimulation rate was increased over the range of 0.5–3 Hz. In fibers stimulated at 1 Hz, cessation of stimulation was immediately followed by an exponential decline of [Formula: see text] with an average time constant of 53 ± 9 s (SD, n = 8), or rate constant of 0.020 ± 0.004/s. Restimulation of the fibers produced an exponential rise of [Formula: see text] with an average time constant of 65 ± 12 s (n = 8). Similar results were obtained in fibers stimulated at 2 Hz. The average rates of rise of [Formula: see text] after the onset of stimulations at 1 and 2 Hz were 1.0 and 1.5 mM/min, equivalent to increments in net sodium influx of 13.2 and 19.8 pmol∙cm−2∙s−1, respectively. The average maximum rate of [Formula: see text] rise produced by the application of 10−5 M strophanthidin to the fibers stimulated at 1 Hz was 1.3 ± 0.5 mM/min, equivalent to a net sodium influx of 17.2 pmol∙cm−2∙s−1.

Acetylcholine increases intracellular sodium activity in sheep cardiac Purkinje fibers

1989 ◽  
Vol 256 (5) ◽  
pp. H1407-H1416
Author(s):  
G. Iacono ◽  
M. Vassalle
Keyword(s):  
Action Potential ◽  
Spontaneous Activity ◽  
Sodium Pump ◽  
Contractile Force ◽  
Intracellular Sodium ◽  
Resting Potential ◽  
Purkinje Fibers ◽  
Transmembrane Potentials ◽  
Sodium Activity ◽  
Cardiac Purkinje Fibers

The action of acetylcholine (ACh) on intracellular sodium activity (alpha iNa) was studied in sheep Purkinje fibers by means of a Na+-selective microelectrode technique while transmembrane potentials and contractile force were simultaneously recorded. In quiescent fibers, 10(-4) to 10(-5) M ACh shifted the resting potential to less negative values and increased alpha iNa from 5.57 +/- 0.21 to 6.45 +/- 0.35 mM (+15.8%, P less than 0.005). In other experiments, ACh induced a depolarization that initiated spontaneous activity. In fibers driven at 60 beats/min, ACh prolonged the action potential, increased alpha iNa from 7.98 +/- 0.15 to 9.36 +/- 0.3 mM (+17.29%, P less than 0.005), and increased contractile force. Norepinephrine (10(-5) to 10(-6) M) increased contractile force and decreased alpha iNa, but in its presence ACh still increased force and alpha iNa and vice versa. Strophanthidin (10(-4) M) increased alpha iNa, and 3 x 10(-6) M propranolol and 10(-6) M atropine decreased alpha iNa. Both strophanthidin and atropine (but not propranolol) prevented the increase in alpha iNa by ACh. It is concluded that the ACh increases alpha iNa and contractile force through the inhibition of the sodium pump and that these actions are due to the activation of the muscarinic receptor and not to endogenously released norepinephrine.

A re-examination of late outward plateau currents of cardiac Purkinje fibers

1985 ◽  
Vol 249 (1) ◽  
pp. H108-H121
Author(s):  
J. M. Jaeger ◽  
W. R. Gibbons
Keyword(s):  
Action Potential ◽  
Voltage Clamp ◽  
Critical Role ◽  
Membrane Current ◽  
Purkinje Fiber ◽  
Purkinje Fibers ◽  
Outward Currents ◽  
Cardiac Purkinje Fibers

Two outward currents, IX1 and IX2, are thought to be activated by depolarization of the Purkinje fiber. One of these, IX1, is presently believed to play a critical role in repolarization of the action potential. The IX currents were originally analyzed in voltage-clamp experiments in sheep Purkinje fibers. These experiments were designed to minimize interference by other currents, and it was assumed that changes of the net current were produced entirely by the IX currents. We have tried to repeat the original experiments and the analysis that led to acceptance of the existence and roles of the IX currents, without success. Moreover, tests of how membrane current should behave if the IX current hypothesis is correct did not give satisfactory results. Our data suggest the original conclusions about IX1 and IX2 may need substantial revision.

Slow inward current may produce many results attributed to IX1 in cardiac Purkinje fibers

1985 ◽  
Vol 249 (1) ◽  
pp. H122-H132
Author(s):  
J. M. Jaeger ◽  
W. R. Gibbons
Keyword(s):  
Action Potential ◽  
Outward Current ◽  
Purkinje Fiber ◽  
Slow Inward Current ◽  
Channel Blockers ◽  
Inward Current ◽  
Purkinje Fibers ◽  
Cardiac Purkinje Fibers ◽  
Current Voltage ◽  
Current Voltage Relation

We have tried to answer two fundamental questions concerning the outward current IX1 of cardiac Purkinje fibers. 1) Is it possible that current changes identified as arising from IX1 in voltage-clamp experiments are actually manifestations of changes in the slow inward current (Isi); and 2) is IX1 in fact required to produce the electrical phenomena attributed to it? Isi behavior and the role of IX1 were explored using computer simulation. The Isi model produced current changes during depolarizations and hyperpolarizations from depolarized resting potentials like those attributed to IX1. It also produced a component of "tail currents" that behaved like IX1. If these current changes were analyzed, assuming that an outward current is responsible, the resulting kinetics and current voltage relation would be very similar to the kinetics and current voltage relation reported for IX1. Using the McAllister, Noble, and Tsien formulation of the Purkinje fiber action potential, we found that IX1 is not essential for repolarization of the reconstructed action potential nor is it needed to reproduce interval duration effects and the effects of applied current in that model. Data suggesting that calcium channel blockers reduce IX1 and that catecholamines increase IX1 may be explained as arising from changes in Isi. Thus many manifestations of IX1 can be explained as arising from unanticipated behavior of Isi, and IX1 does not necessarily play a key role in generating Purkinje fiber electrical activity.

scholarly journals Effect of Formaldehyde and Glutaraldehyde on Electrical Properties of Cardiac Purkinje Fibers

1969 ◽  
Vol 53 (5) ◽  
pp. 530-540 ◽  
Author(s):  
H. A. Fozzard ◽  
G. Dominguez
Keyword(s):  
Action Potential ◽  
Negative Charge ◽  
Input Resistance ◽  
Membrane Resistance ◽  
Rapid Loss ◽  
Purkinje Fibers ◽  
Electrophysiological Properties ◽  
Cardiac Purkinje Fibers ◽  
Length Constant ◽  
Upstroke Velocity

The effects of formaldehyde, glutaraldehyde, 1-fluoro-2,4-dinitrobenzene, and 1,5-difluoro-2,4-dinitrobenzene on the electrophysiological properties of cardiac Purkinje fibers were studied. At concentrations of 2.5 mM the aldehydes produced a transient hyperpolarization, lengthening of the plateau of the action potential, and an increase in action potential overshoot and upstroke velocity. If exposure to aldehyde was continued, the fiber failed to repolarize after an action potential and the membrane potential stabilized at about -30 mv. If exposure was terminated before this, recovery was usually complete. At the time the fibers were hyperpolarized the input resistance was increased without much change in length constant, leading to an increase in both calculated membrane resistance and calculated core resistance. Although it was anticipated that an effect of the aldehydes on the membrane was to increase fixed negative charge, it was difficult to explain all the electrophysiological changes on this basis. The major effects of the fluorobenzene compounds were not the same; they produced a shortening of the action potential and a rapid loss of excitability.

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