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Actions of Diphenylhydantoin on the Electrical Properties of Isolated Rabbit and Canine Atria
The effects of diphenylhydantoin (DPH), 10 to 10M, were studied on the various types of cells in the isolated right atrial preparation and on the specialized cells of Bachmannʼs bundle in atrial preparations obtained from puppies. High concentrations of DPH (10M) slowed sinoatrial rate but lower con...
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Published in: | Circulation research 1968-09, Vol.23 (3), p.463-477 |
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Main Authors: | , , , |
Format: | Article |
Language: | English |
Citations: | Items that cite this one |
Online Access: | Get full text |
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Summary: | The effects of diphenylhydantoin (DPH), 10 to 10M, were studied on the various types of cells in the isolated right atrial preparation and on the specialized cells of Bachmannʼs bundle in atrial preparations obtained from puppies. High concentrations of DPH (10M) slowed sinoatrial rate but lower concentrations had little effect. These chronotropic effects of DPH were direct. DPH in concentrations above 10M decreased the slope of phase 4 depolarization in cells in the sinoatrial node and venous automatic tissue. DPH in concentrations of 10 to 10M had no effect on transmembrane action potentials recorded from any cell studied; concentrations of 10M, however, prolonged the terminal phase of repolarization. High concentrations (10M) also prolonged the effective refractory period of Bachmannʼs bundle and ordinary atrial and perinodal fibers by an average of 10%. DPH markedly increased the dv/dt of phase 0 of the action potential and membrane responsiveness of ordinary atrial and specialized Bachmannʼs bundle fibers under control conditions and produced more striking increases when these two variables had been decreased by ouabain. DPH was also proved capable of reversing ouabain-induced sinoatrial block. This unique ability of DPH to enhance membrane responsiveness and to improve conduction in the absence of significant effects on the effective refractory period and automaticity of atrial cells suggests that this may be the sole mechanism of its antiarrhythmic action. |
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ISSN: | 0009-7330 1524-4571 |
DOI: | 10.1161/01.res.23.3.463 |