scholarly journals A study of the effect of the rate of stimulation on the transient outward current in sheep cardiac Purkinje fibres.

1981 ◽  
Vol 319 (1) ◽  
pp. 1-22 ◽  
Author(s):  
M R Boyett
Keyword(s):  
Outward Current ◽  
Transient Outward Current ◽  
Purkinje Fibres ◽  
Cardiac Purkinje Fibres

Role of intracellular calcium in the transient outward current of calf Purkinje fibres

Nature ◽  
1977 ◽  
Vol 269 (5629) ◽  
pp. 611-613 ◽  
Author(s):  
S. A. SIEGELBAUM ◽  
R. W. TSIEN ◽  
R. S. KASS
Keyword(s):  
Intracellular Calcium ◽  
Outward Current ◽  
Transient Outward Current ◽  
Purkinje Fibres

Mechanisms underlying the shortening of the action potential at high and low stimulus rates in sheep Purkinje fibres

1985 ◽  
Vol 225 (1241) ◽  
pp. 481-502 ◽  
Keyword(s):  
Action Potential ◽  
Stimulus Frequency ◽  
Outward Current ◽  
Transient Outward Current ◽  
Purkinje Fibres ◽  
High Frequencies ◽  
Pacemaker Potential ◽  
K Concentration ◽  
Diastolic Potential ◽  
Action Potential Shortening

The shortening of the action potential of sheep Purkinje fibres at high and low rates of stimulation has been investigated. The shortening of the action potential at high rates can be entirely accounted for by incomplete recovery of the plateau conductances between beats. When sufficient time is allowed for membrane recovery, a prolongation of the action potential, rather than a shortening, occurs at high frequencies. The effect on electrical activity of increasing the stimulus frequency is similar to decreasing the bathing K concentration. The possibility of a reduction in the cleft K concentration at high frequencies is discussed. The shortening of the action potential at low rates is unaffected by 4-amino pyridine (a blocker of the transient outward current, i to ) is abolished by D600 (a blocker of the second inward current, i st ) and by a rise in the bathing Ca concentration. It is concluded that i si rather than i to is involved in action potential shortening at low rates. Action potential shortening at low rates is closely associated with declines in the maximum diastolic potential and the pacemaker potential; all of these changes are abolished by ouabain (a blocker of the Na-K pump). It is concluded that the shortening of the action potential at low rates may be the result of a decline in i si , which in turn is dependent on a decline in [Na] i . It is suggested that the rate-dependent changes in the maximum diastolic potential, pacemaker potential and tension are also related to [Na] i .

Regional Differences in Transient Outward Current Density and Inhomogeneities of Repolarization in Rabbit Right Atrium

Circulation ◽  
1995 ◽  
Vol 92 (10) ◽  
pp. 3061-3069 ◽  
Author(s):  
Takeshi Yamashita ◽  
Toshiaki Nakajima ◽  
Hisanori Hazama ◽  
Eiji Hamada ◽  
Yuji Murakawa ◽  
...  
Keyword(s):  
Current Density ◽  
Right Atrium ◽  
Regional Differences ◽  
Outward Current ◽  
Transient Outward Current

scholarly journals Endurance exercise training normalizes repolarization and calcium-handling abnormalities, preventing ventricular fibrillation in a model of sudden cardiac death

2012 ◽  
Vol 113 (11) ◽  
pp. 1772-1783 ◽  
Author(s):  
Ingrid M. Bonilla ◽  
Andriy E. Belevych ◽  
Arun Sridhar ◽  
Yoshinori Nishijima ◽  
Hsiang-Ting Ho ◽  
...  
Keyword(s):  
Sudden Cardiac Death ◽  
Exercise Training ◽  
Endurance Exercise ◽  
Cardiac Death ◽  
Outward Current ◽  
Calcium Handling ◽  
Transient Outward Current ◽  
Cellular Electrophysiology ◽  
Endurance Exercise Training

The risk of sudden cardiac death is increased following myocardial infarction. Exercise training reduces arrhythmia susceptibility, but the mechanism is unknown. We used a canine model of sudden cardiac death (healed infarction, with ventricular tachyarrhythmias induced by an exercise plus ischemia test, VF+); we previously reported that endurance exercise training was antiarrhythmic in this model (Billman GE. Am J Physiol Heart Circ Physiol 297: H1171–H1193, 2009). A total of 41 VF+ animals were studied, after random assignment to 10 wk of endurance exercise training (EET; n = 21) or a matched sedentary period ( n = 20). Following (>1 wk) the final attempted arrhythmia induction, isolated myocytes were used to test the hypotheses that the endurance exercise-induced antiarrhythmic effects resulted from normalization of cellular electrophysiology and/or normalization of calcium handling. EET prevented VF and shortened in vivo repolarization ( P < 0.05). EET normalized action potential duration and variability compared with the sedentary group. EET resulted in a further decrement in transient outward current compared with the sedentary VF+ group ( P < 0.05). Sedentary VF+ dogs had a significant reduction in repolarizing K+ current, which was restored by exercise training ( P < 0.05). Compared with controls, myocytes from the sedentary VF+ group displayed calcium alternans, increased calcium spark frequency, and increased phosphorylation of S2814 on ryanodine receptor 2. These abnormalities in intracellular calcium handling were attenuated by exercise training ( P < 0.05). Exercise training prevented ischemically induced VF, in association with a combination of beneficial effects on cellular electrophysiology and calcium handling.

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