1988 Fiscal Year Final Research Report Summary
Mechanism of appearance of periodic variation of arrhythmias
| Project/Area Number |
61570424
|
|---|
| Research Category |
Grant-in-Aid for General Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Circulatory organs internal medicine
|
|---|
| Research Institution | Kyushu University |
|---|
Principal Investigator |
TAKASHI YANAGA Professor, Department of Bioclimatology and Medicine, Medical Institute of Biore, 生体防御医学研究所, 教授 (80038702)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
YUHEI ICHIMARU Assistant, Department of Bioclimatology and Medicine, Medical Institute of Biore, 生体防御医学研究所, 助手 (70038909)
NAOKI MAKINO Lecturer, Department of Bioclimatology and Medicne, Medical Institute of Bioregu, 生体防御医学研究所, 講師 (60157170)
|
|---|
| Project Period (FY) |
1986 – 1988
|
| Keywords | Acoustic stimuli / Catecholamine / Bradyarrhythmias / Periodic Variation / Sudden death / カテコールアミン / Ca拮抗剤 |
|---|
| Research Abstract |
The mechanism of apperance of apperarance of periodic variation of arrhythmias, especially of malignant arrhythmias, was studied in rabbits and rats. The results were as follows;
1) Experimental model of malignant arrhythmias. The electrocardiogram was recorded by telemetry for abut 11 days in unrestricted rabbits. Severe bradyarrhythmias were induced by acoustic stimuli in the setting of high level of serum catecholamine. sudden death was observed in one rabbit.
2) Relationship between coupling interval and appearance of ventricular tachycardia or fibrillation Digitalis-induced arrhythmias were observed in rabbits. Coupling interval of initial QRS complex of lethal arrhythmias decreased at the presence of high serum calcium and increased after the administration of Ca^<2+> channel blocker.
3)Modulation of Na^+-Ca^<2+> exchange in cardiac sarcolemmal vesicles by Ca^<2+>antagonist the effect of Ca^<2+> antagonist on the Na^+-dependent Ca^<2+> uptake was studied in sarcolemmal vesicles in rats. None of the agents depressed the initial rate of Ca^<2+>uptake until concentration of 10 m were incubated in the incubation medium. However, when sarcolemmal vesicles were preloaded with Ca^<2+> via ATP-dependent Ca^<2+> uptake, cellular Ca^<2+> influx was depressed only by verapamil. The order of Ca^<2+> efflux was verapamil>diltiazem>nifedipine. Above results suggest that acoustic stimuli in the presence of high serum catecholamine are involved in the appearance of malignant arrhythmias, and abnormalities in Na^+-Ca^<2+> exchange are involved in the mechanism of demage of myocardial cell.
|
