scholarly journals Relationships between voltage and tension in sheep cardiac Purkinje fibers.

1975 ◽  
Vol 65 (3) ◽  
pp. 345-365 ◽  
Author(s):  
W R Gibbons ◽  
H A Fozzard

The two-microelectrode technique of voltage clamping sheep cardiac Purkinje fibers was used to examine the changes in contraction which occur during trains of voltage clamps. (A "train" is defined as a series of voltage clamps delivered at a particular rate, beginning after a rest long enough that the effects of previous stimulation have died away.) Contractions showed striking staircases, or progressive changes in peak isometric tension, during trains. Short clamps, clamps to voltages more negative than --20 or --30 mV, or holding potentials less negative than the resting potential favored negative staircases, while long clamps, clamps to positive voltages, and holding potentials near the resting potential each favored positive staircases. The staircase behavior appeared to be due to changes in the initial rate of recovery of the ability to contract. The changes in staircase behavior as a function of clamp voltage suggested that the relationship between peak tension and clamp voltage should depend on the experimental design. When the steady-state contraction was plotted as a function of clamp voltage, voltage-tension relations like those recently reported for working ventricle were obtained, with a threshold between --30 and --40 mV and a steep relation between tension and voltage. When the first contraction after a rest was plotted, the threshold voltage was more negative, the curve was flatter, and the peak tensions at inside positive voltages were reduced.

1997 ◽  
Vol 272 (4) ◽  
pp. H1826-H1832 ◽  
Author(s):  
R. F. Gilmour ◽  
N. F. Otani ◽  
M. A. Watanabe

The contribution of cumulative changes in action potential duration (memory) to complex cellular electrophysiological behavior was investigated in canine cardiac Purkinje fibers. Complex behavior induced during constant pacing was caused by reciprocal interactions between the time to full repolarization (TFR), where TFR = response duration + latency, and the diastolic interval (DI). The relationship between TFR and the preceding DI during complex behavior differed from that obtained using a standard restitution protocol. In particular, higher-order periodicities and chaos were produced in fibers in which the restitution curve lacked the prerequisites for such behavior. To investigate whether shifts in the restitution curve might be expected during rapid pacing, the relationship between TFR of a test response (TFR(n + 1)) and the immediately preceding response (TFR(n)) was determined. For any fixed DI(n), reduction of TFR(n) from 240 to 130 ms was accompanied by a corresponding reduction of TFR(n + 1), whereas as TFR(n) was reduced further to 120 ms, TFR(n + 1) increased. Because of the dependence of TFR(n + 1) on TFR(n) (memory) and on the preceding DI(n) (restitution), the slope of the low-dimensional relationship between TFR(n + 1) and DI(n) at a constant pacing cycle length depended on the slopes of the restitution and memory functions. These results suggest that rapid accumulation and dissipation of memory may contribute importantly to complex electrical behavior in cardiac tissue.


1982 ◽  
Vol 243 (1) ◽  
pp. H77-H86 ◽  
Author(s):  
S. L. Lipsius ◽  
W. R. Gibbons

We examined relationships between isometric tension and membrane currents in sheep Purkinje fibers voltage clamped by the two-microelectrode method. Oscillatory restitution of contractility was accompanied by a small oscillation in membrane current and by an aftercontraction. The membrane current oscillation resembled the transient inward current (TI) others have reported in the presence of strophanthidin. Twitches produced by voltage clamp depolarizations did not correlate with net outward current in normal solution, but when the early outward current was blocked by 0.5 mM 4-aminopyridine, the residual outward current did correlate with twitches elicited by strong depolarizing clamps, particularly in solutions containing higher than normal calcium concentrations. The results illustrate important similarities and differences between membrane current behavior in sheep Purkinje fibers and behavior others have reported in calf fibers. Correlations between restitution, aftercontractions, and TI's, and between twitch tension and a component of outward current, may arise because of calcium regulation of membrane conductance, electrogenic Na-Ca exchange, or a combination of these and other mechanisms.


1980 ◽  
Vol 238 (4) ◽  
pp. H561-H568
Author(s):  
S. R. Houser ◽  
A. R. Freeman

Volumetric properties of canine cardiac Purkinje fibers were examined. Purkinje cells were superfused with anisosmolar solutions, and changes in extracellular space and relative cell volume were determined. The relationship between cellular volume and the osmolarity of the bathing medium was shown to be linear except in solutions of very low osmolarity. A linear regression line crossed the volume axis at 38%, suggesting an osmometric dead space of 38% and correspondingly an osmometric compartment comprising about 62% of the cell interior. To determine the volumetric properties of the "electrophysiological compartment," Purkinje cells were impaled with voltage-sensitive microelectrodes, and cellular resting potentials were recorded. When log K was plotted against resting potential (Em) in preparations bathed in normal and hyperosmotic solutions, it was shown that Em was increased in hyperosmotic solutions (13.5 and 21 mV in 600 and 850 mosM solutions, respectively). Calculations using the Nernst equation showed that the compartment containing the intracellular K involved in membrane electrical events behaves as a near-perfect osmometer in hyperosmotic solutions. Changes in the osmometric compartment were well correlated with K changes in the electrophysiological compartment, thus suggesting that the K is homogeneously distributed intracellularly.


1974 ◽  
Vol 64 (4) ◽  
pp. 473-493 ◽  
Author(s):  
Jay R. Wiggins ◽  
Paul F. Cranefield

Canine cardiac Purkinje fibers exposed to Na-free solutions containing 128 mM TEA and 16 mM Ca show resting potentials in the range -50 to -90 mV; if the concentration of Na in the perfusate is raised from 0 to 4 to 24 mM, hyperpolarization follows. If the initial resting potential is low, the hyperpolarization tends to be greater; the average increase in the presence of 8 mM Na is 14 mV. Such hyperpolarization is not induced by adding Na to K-free solutions, is not seen in cooled fibers, or in fibers exposed to 10-3 M ouabain, nor is it induced by adding Li and thus may result from electrogenic sodium extrusion. Fibers exposed to Na-free solutions are often spontaneously active; if they are quiescent they often show repetitive activity during depolarizing pulses. Such spontaneous or repetitive activity is suppressed by the addition of Na. This suppression may or may not be related to the hyperpolarization.


1987 ◽  
Vol 252 (3) ◽  
pp. H645-H652 ◽  
Author(s):  
R. M. Terek ◽  
C. T. January

Oscillatory afterpotentials, or late afterdepolarizations, are one mechanism postulated to cause cardiac arrhythmias and possibly conduction disturbances. We studied excitability by determining strength-interval curves in Purkinje fibers under normal conditions and during the presence of oscillatory afterpotentials induced by cardiac glycoside toxicity. During exposure to acetylstrophanthidin (0.10–0.15 mg/l), the mean resting potential depolarized 5.6 mV and oscillatory afterpotentials of 3–17 mV appeared. Current threshold for evoking action potentials was reduced below control level (e.g., increased excitability) throughout electrical diastole. Associated with oscillatory afterpotentials was a marked biphasic variation in current threshold giving strength-interval curves a characteristic biphasic shape. During the rising phase of the oscillatory afterpotentials, excitability reached a maximum, whereas the minimum increase in excitability occurred during the falling phase of oscillatory afterpotentials. This biphasic change in excitability remained correlated with the oscillatory afterpotentials at different cycle lengths. Results show that during acetylstrophanthidin toxicity excitability is increased throughout electrical diastole, and characteristic time-dependent changes in excitability occur during oscillatory afterpotentials. Time-dependent changes in excitability were detected with both intra- and extracellular stimulation techniques.


1983 ◽  
Vol 61 (11) ◽  
pp. 1329-1339 ◽  
Author(s):  
Cheng-I Lin ◽  
Mario Vassalle

In cardiac Purkinje fibers, strophanthidin increases and then decreases contractile force. The relationship between the decrease in force and calcium overload was studied by recording the electrical and mechanical activity under conditions known to increase calcium overload or its effects. Inhibitors of oxidative phosphorylation reduced the positive inotropy of strophanthidin and enhanced the decrease in force. These inhibitors also reduced the inotropic effect of high calcium. Increasing intracellular calcium by decreasing extracellular sodium concentration also resulted in a decrease in the strophanthidin inotropy. When arrhythmia was delayed, strophanthidin induced contracture and this was favored by blockers of glycolysis and by enhancing cellular calcium. Some of these effects were also observed in ventricular muscle fibers but at higher strophanthidin concentrations. The results suggest that the decline in contractile force during strophanthidin exposure is related to calcium overload, although it is made clear that in Purkinje fibers contractile force and resting force may be independently affected under suitable conditions.


1994 ◽  
Vol 267 (2) ◽  
pp. H725-H733 ◽  
Author(s):  
J. Sprung ◽  
D. F. Stowe ◽  
J. P. Kampine ◽  
Z. J. Bosnjak

Mild hypothermia enhances cardiac contractility, and volatile anesthetics depress contractility. Contractile force (tension) and Ca2+ transients were measured in canine Purkinje fibers at 35 and 25 degrees C with and without halothane and isoflurane to examine how anesthetics attenuate the positive inotropic effect of mild hypothermia. Isometric tension and light emitted from the photoprotein aequorin were used to assess contractility and intracellular Ca2+ transients in fibers stimulated at 40–60 pulses/min. At 35 degrees C, each anesthetic depressed peak tension and peak Ca2+ transients and decreased contractile force duration but, for halothane, increased Ca2+ transient duration. Decreases in tension by both anesthetics at 35 degrees C were converted to marked increases in tension at 25 degrees C, whereas Ca2+ transients were little changed. Removal of anesthetics at 25 degrees C greatly increased tension with a small increase in Ca2+ transients that was much lower than that at 35 degrees C. The curve relating peak contractile force as a function of Ca2+ transients at 25 degrees C during stepwise increases in extracellular CaCl2 was shifted steeper and leftward of the curve at 35 degrees C. These studies suggest that the positive inotropic effect of mild hypothermia is due primarily to increased myofibrillar Ca2+ sensitivity and that anesthetics decrease tension during hypothermia by decreasing myofibrillar Ca2+ sensitivity. Reduced influx of transsarcolemmal or sarcoplasmic reticular Ca2+ may also play a role during mild hypothermia.


1989 ◽  
Vol 256 (5) ◽  
pp. H1407-H1416
Author(s):  
G. Iacono ◽  
M. Vassalle

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.


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