| Project/Area Number |
13670737
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Circulatory organs internal medicine
|
|---|
| Research Institution | Kyoto Prefectural University of Medicine |
|---|
Principal Investigator |
TANAKA Hideo Kyoto Prefectural University of Medicine, Assistant, 医学部, 助手 (60236619)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
TAKAMATSU Tetsuro Kyoto Prefectural University of Medicine, Professor, 医学部, 教授 (40154900)
|
|---|
| Project Period (FY) |
2001 – 2002
|
| Project Status |
Completed (Fiscal Year 2002)
|
| Budget Amount *help |
¥2,700,000 (Direct Cost: ¥2,700,000)
Fiscal Year 2002: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2001: ¥2,000,000 (Direct Cost: ¥2,000,000)
|
|---|
| Keywords | acute myocardial infarction / confocal microscopy / metabolic inhibition / arrhythmia / calcium wave |
|---|
| Research Abstract |
Although abnormal [Ca^<2+>]_1 dynamics at ischemic border zone myocardium causes various complications in acute myocardial infarction, its cellular aspects remain uncertain. Real-time confocal [Ca^<2+>]_1 dynamics were visualized at epicardial border zones (EBZ) of rat myocardial infarcts loaded with fluo 3/AM under 2-hr coronary occlusion. EBZ exhibited no spatially homogeneous Ca^<2+> transients. Instead, two types of intracellular Ca^<2+> waves emerged at two different regions; the adjacent region adjoining. The infarctedmargin and its surrounding vicinity. The waves at the vicinity emerged synchronously upon Ca^<2+> transients, whereas those at the adjacent region arose independently of ventricular exsitation Ca^<2+> waves (n=78) at the adjacent regions exhibited more frequently (17.6 ^^+__- 10.7 waves/min/cell) and with more rapid intracellular propagation (the propagation velocity was 198.4 ^^+__- 42.6 um/s) than those (n=76) at the visinity (7.1 ^^+__- 4.6 waves/min/cell and 140.8 ^^+__- 31.2 um/s, respectively). On time-lapse analysis these parameters decreased sequenially with quicker decline at the adjacent regions than at the vicinities. The accompanying disappearance of the waves resulted in patchy distribution of quiescent myocytes showing neither [Ca^<2+>]_1 fluctuations nor high-static [Ca^<2+>]_1. Isoproterenol reversed the sequential decline at the vicinities but not at the adjacent regions. Histochemistry for succinate dehydrogenase (reflecting mitochondrial ATP production) indicated close relevance to the spatial inhomogeneity of [Ca^<2+>]_1 dynamics. These data are the first to provide cellular aspects of abnormal [Ca^<2+>]_1 dynamics within EBZ of acute myocardial infarct. The inhomogeneous distribution of Ca^<2+> waves and quiescent myocytes, determined by both [Ca^<2+>]_1 loading and metabolic conditions, would contribute to electromechanical dysfunction that occur during acute myocardial infarction
|
