Heart failure in hypertrophied hearts - myocyte apoptosis produced by ischemia-reperfusion
Project/Area Number |
10670626
|
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 | Tohoku Buna Gakuen University (1999) Tohoku University (1998) |
Principal Investigator |
ISOYAMA Shogen Tohoku Bunka Gakuen University, Faculty of Medical Science & Welfare, Professor, 医療福祉学科, 教授 (10133943)
|
Project Period (FY) |
1998 – 1999
|
Project Status |
Completed (Fiscal Year 1999)
|
Budget Amount *help |
¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1999: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1998: ¥1,000,000 (Direct Cost: ¥1,000,000)
|
Keywords | myocardial hypertorphy / myocytes / apoptosis / ischemia / ACE inhibitor / 肥大心 / 心筋 / Bax蛋白 / 心不全 |
Research Abstract |
The heart responds to arterial hypertension with myocardial hypertrophy. However, when the overload lasts longer, hypertrophied hearts are led to failure. Several mechanisms responsible for the transition from compensation to failure in hypertrophied hearts have been raised: attenuated expression of genes such as heat shock proteins and heme oxygenase. It is generally accepted that hypertrophied hearts are susceptible to ischemia because of decreased coronary flow reserve. In this study, we tested the hypothesis that the myocyte apoptosis is more frequently produced by ischeniia and the apoptosis is responsible for the transition in hypertrophied hearts. We divided rats into two groups: the group hypertrophied by ascending aortic banding (n=18) and the control group (n=18). Four weeks after ascending aortic banding, the chest was again opened under general anesthesia, and a snare of a nylon thread was put around the left coronary artery. Coronary occlusion was applied by tightening the
… More
snare for 10 minutes in the two groups of rats, and the chest was closed. The hearts were excised at 0, 3 and 6 hours of reperfusion for analysis of Bax protein expression and myocyte apoptosis by the immunohistochemical technique and Tunnel method, respectively. The ratio of left ventricular weight to body weight (mg/g) in the hypertrophied group was 3.1±0.4 and significantly greater that that in the control group (2.4 ± 0.2). At 0 hours of reperfusion apoptotic myocytes were not detected in the two groups, but detected more frequently in the hyperrophied group than in the control group at 3 and 6 hours (0.16±0.14 vs. 0.04±0.01% at 3 hours; 0.15±0.02 vs. 0.01±0.01% at 6 hours). The expression of Bax protein was decreased in the hypertcophied group before and after applying the ischemic insult, compared with the control group. Conclusion: Apoptosis was more frequently induced by ischemia/reperfision insult in hypertrophied myocytes. Bax protein was rather less expressed in hypertrophied hearts. This protein does not play an important role in inducing myocyte apoposis in hypertrophied hearts. The chronic treatment with an angiotensin-converting-enzyme inhibitor, cilazapril, restored the attenuated expression of heat shock proteins, and heme oxygenase, but did not affect the myocyte apoptosis. Less
|
Report
(3 results)
Research Products
(7 results)