scholarly journals Electrophysiological effects of bunaftine, an antiarrhythmic drug, on action potential characteristics in ventricular muscle preparations.

1986 ◽  
Vol 88 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Takahito KIMURA ◽  
Mikio NAKAZAWA ◽  
Shoichi IMAI
1978 ◽  
Vol 56 (1) ◽  
pp. 139-149 ◽  
Author(s):  
Teresa Kus ◽  
Betty I. Sasyniuk

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.


1999 ◽  
Vol 277 (2) ◽  
pp. H826-H833 ◽  
Author(s):  
Seiko Tanabe ◽  
Toshio Hata ◽  
Masayasu Hiraoka

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.


1960 ◽  
Vol 198 (6) ◽  
pp. 1143-1147 ◽  
Author(s):  
Chandler McC. Brooks ◽  
Jerome L. Gilbert ◽  
Martin E. Greenspan ◽  
Gertrude Lange ◽  
Hector M. Mazzella

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.


2012 ◽  
Vol 118 (4) ◽  
pp. 506-511 ◽  
Author(s):  
Akira Takahara ◽  
Kiyoshi Takeda ◽  
Yayoi Tsuneoka ◽  
Mihoko Hagiwara ◽  
Iyuki Namekata ◽  
...  

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