Differential Effects of Halothane and Isoflurane on Contractile Force and Calcium Transients in Cardiac Purkinje Fibers

1994 ◽  
Vol 80 (6) ◽  
pp. 1360-1368 ◽  
Author(s):  
David F. Stowe ◽  
Juraj Sprung ◽  
Lawrence A. Turner ◽  
John P. Kampine ◽  
Zeljko J. Bosnjak
Keyword(s):  
Contractile Force ◽  
Calcium Transients ◽  
Purkinje Fibers ◽  
Differential Effects ◽  
Cardiac Purkinje Fibers

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.

Calcium overload and strophanthidin-induced mechanical toxicity in cardiac Purkinje fibers

1983 ◽  
Vol 61 (11) ◽  
pp. 1329-1339 ◽  
Author(s):  
Cheng-I Lin ◽  
Mario Vassalle
Keyword(s):  
Sodium Concentration ◽  
Contractile Force ◽  
Calcium Overload ◽  
Mechanical Activity ◽  
Ventricular Muscle ◽  
Purkinje Fibers ◽  
Cardiac Purkinje Fibers ◽  
High Calcium ◽  
Extracellular Sodium ◽  
The Relationship

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.

Hypothermia modifies anesthetic effect on contractile force and Ca2+ transients in cardiac Purkinje fibers

1994 ◽  
Vol 267 (2) ◽  
pp. H725-H733 ◽  
Author(s):  
J. Sprung ◽  
D. F. Stowe ◽  
J. P. Kampine ◽  
Z. J. Bosnjak
Keyword(s):  
Positive Inotropic Effect ◽  
Mild Hypothermia ◽  
Cardiac Contractility ◽  
Volatile Anesthetics ◽  
Contractile Force ◽  
Isometric Tension ◽  
Inotropic Effect ◽  
Purkinje Fibers ◽  
Peak Tension ◽  
Cardiac Purkinje Fibers

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.

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.

Effect of calcium on strophanthidin-induced electrical and mechanical toxicity in cardiac Purkinje fibers

1979 ◽  
Vol 236 (5) ◽  
pp. H689-H697 ◽  
Author(s):  
M. Vassalle ◽  
C. I. Lin
Keyword(s):  
Therapeutic Effect ◽  
Contractile Force ◽  
Purkinje Fibers ◽  
Subsequent Decrease ◽  
Cardiac Purkinje Fibers ◽  
High Calcium ◽  
Normal Calcium ◽  
Excessive Accumulation

The role of calcium in the electrical and mechanical toxicity induced by strophanthidin (10(-6) M) was studied in canine Purkinje fibers perfused in vitro. Strophanthidin caused an increase in contractile force ("therapeutic effect") followed by a subsequent decrease and by the onset of arrhythmias ("toxic effects"). The onset of arrhythmias occurred sooner in low- and later in high-calcium solutions with respect to the normal calcium. The positive inotropic (therapeutic) effect of strophanthidin was reduced or prevented by caffeine (1 mM) or by high calcium. The late (toxic) decline in force during exposure to strophanthidin was temporarily reversed by decreasing [Ca]o to a low value. Similarly, the contractile force decreased when [Ca]o was increased from 8.1 to 16.2 mM and this decline was transiently reversed when [Ca]o was reduced to a low value. It is concluded that in Purkinje fibers 1) electrical toxicity may occur independently of an intracellular calcium accumulation, and 2) the mechanical toxicity may be due to an excessive accumulation of calcium in the fiber.

Inhibitory effects of catecholamines in canine cardiac Purkinje fibers

1976 ◽  
Vol 231 (5) ◽  
pp. 1415-1420 ◽  
Author(s):  
P Posner ◽  
EL Farrar ◽  
CR Lambert
Keyword(s):  
Negative Response ◽  
Chronotropic Effect ◽  
Inhibitory Effects ◽  
Purkinje Fibers ◽  
Spontaneous Rate ◽  
Negative Chronotropic Effect ◽  
Cardiac Purkinje Fibers ◽  
Wide Range ◽  
Low Levels

The effect of catecholamines over a wide range of concentrations was studied on 42K uptake and efflux, as well as on spontaneous rate in canine cardiac Purkinje fibers. Low levels of catecholamines (less than 10(-10) M epinephrine; less than 10(-9) M norepinephrine) decreased automaticity. This negative chronotropic effect was blocked by phentolamine and mimicked by phenylephrine. These low levels of epinephrine and norepinephrine also inhibited 42K uptake by Purkinje fibers but had no effect on 42K efflux. The inhibition of 42K uptake was blocked by phentolamine and verapamil and mimicked by phenylephrine. The data indicate an alpha-receptor-mediated negative response of rate and 42K uptake to low levels of catecholamine. The end result is discussed in terms of a competitive increase in the influx of Ca2+ rather than Na+ and an indirect inhibition of the Na+-K+ pump.

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