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GINMU >
03 紀要 >
031 Journal of Nara Medical Association >
Vol.46 No.2 >
Please use this identifier to cite or link to this item:
http://hdl.handle.net/10564/801
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| Title: | PROARRHYTHMIC ACTIONS OF CLASS Ⅲ ANTIARRHYTHMIC DRUGS IN RABBIT SINO-ATRIAL NODAL CELLS |
| Authors: | Satoh, Hiroyasu |
| Keywords: | class Ⅲ antiarrhythmic drugs
proarrhythmic action
intracellular Ca2+ concentration
calcium overload
transient inward current |
| Issue Date: | 30-Apr-1995 |
| Publisher: | 奈良医学会 |
| Citation: | 奈良医学雑誌 Vol.46 No.2 p.63-74 |
| Abstract: | Arrhythmias induced by class Ⅲ antiarrhythmic drugs (amiodarone,
bretylium and sotalol) in spontaneously beating rabbit sino-atrial nodal cells were inves-
tigated using voltage-clamp and Ca2+ -sensitive fluorescent dye (fura-2). These drugs
caused a negative chronotropic effect, and amiodarone and sotalol prolonged the action
potential duration. Amiodarone (10μM) induced arrhythmias in 3 out of 10 cells, and
simultaneously elicited a transient inward current. Bretylium (10μM) increased the
incidence of arrhythmias in 5 out of 11 cells, and sotalol (10μM) caused arrhythnias in only
one of 10 cells. These drugs inhibited the Ca2+ and delayed rectifier K+ and hyperpolariza-
tion-activated inward currents. The kinetics for activation and inactivation of these
currents were unaffected. After a washout, the regular rhythm was resumed and the
transient inward current also disappeared. Change in the cytosolic Ca2+ concentration was
monitored with fura-2. Amiodarone (10-30 μM) and bretylium (0.1-10 μM) significantly
elevated the cytosolic Ca2+ level, but sotalol, even at 1mM, did not affect it. These results
indicate that the class Ⅲ antiarrhythmic drugs possess proarrhythmic actions, probably
resulting from elevation of cellular Ca2+ concentration as well as the prolongation of action
potential. |
| URI: | http://hdl.handle.net/10564/801 |
| ISSN: | 04695550
13450069 |
| Appears in Collections: | Vol.46 No.2
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| 063-074p.PROARRHYTHMIC ACTIONS OF CLASS Ⅲ ANTIARRHYTHMIC DRUGS.pdf | | 1159Kb | Adobe PDF | View/Open |
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