1998 Fiscal Year Final Research Report Summary
Electrophysiological properties of arryhthmic aggravation by various antiarrhythmic drugs
| Project/Area Number |
09670705
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Medical Research Institute, Tokyo Medical and Dental University |
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Principal Investigator |
SAWANOBORI Tohru Tokyo Medical and Dental University, Medical Research Institute, Professor, 難治疾患研究所, 教授 (00014217)
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| Co-Investigator(Kenkyū-buntansha) |
HIRAOKA Masayasu Medical Research Institute, Professor, 難治疾患研究所, 教授 (80014281)
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| Project Period (FY) |
1997 – 1998
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| Keywords | antiarrhythmic drug / proaarrhythmia / rabbit right atrium / reentrant tachycardia / effective refractroy period / echo zone / microelectrode method / aggravation of existing arrhythmias |
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| Research Abstract |
The goal of this study was to investigate the aggravation factor and electrophysiological mechanisums of the proarrhythmic effect of each different antiarrhythmic drug in the rabbit right atrium. Programmed electrical stimulation a using single premature stimulus was used to obtain the inducebility of reentrant tachycardia both during control and administration of antiarrhythmic drugs. During control, application of a premature stimulus did not induce reentrant tachycardia in all 39 preparations. Administration of 1O^<-7> g/ml acechylcholine induced reentrant tachycardia in 3 out of 6 preparations. Slight incision on reentrant circuit produced the tachycardia in 19 out of 31 preparations. In latter preparation, during each administration of disopyramide, flecainide, mexiletine, sernatilide and bepridil, aggravation of reentrant tachycardia was induced in 4 out of 5, 3 Out of 6, 0 out of 6, 3 out of 8, and I out of 4 preparations, respectively. The aggravation is of arrhythmia in each was, inhibited in later time. Suppressed preparations of stimulus-induced reentrant tachycardia during administration of antiarrhythmic drugs widened the difference between the minimum value of echo zone, and effective refractory period (ERP). Aggravation of reentrant tachycardia was induced rather in therapeutic dose than in high doses except the case of bepridil. Dispersion of ERP was increased in aggravated cases. These results indicate that the changes of ERP and time course of the excitation process are contributed to the aggravation of existing arrhythmias due to drug concentration and the exposure time of the drug.
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