| Autor: |
Zhang, Mei, Elkassem, Samer, Davidoff, Allen, Saito, Kaoru, ter Keurs, Henk |
| Zdroj: |
Molecular and Cellular Biochemistry; September 2003, Vol. 251 Issue: 1-2 p111-117, 7p |
| Abstrakt: |
Hypertrophy and heart failure following a myocardial infarction in rodents are accompanied by a switch of myosin isoforms from V1to V3. The angiotensin II receptor blocker, Losartan, has been demonstrated to improve cardiac function and long-term survival after myocardial infarction. In this study we have investigated whether chronic Losartan treatment affects myosin isoform composition in the hearts of rats following a myocardial infarction. Rats were subjected to coronary artery ligation and received either Losartan (1 g/L) in the drinking water or water only. Four months after myocardial infarction, rats were classified as having either congestive heart failure (cMI) or uncomplicated myocardial infarction (uMI) based on their lung weight to body weight ratio (LW/BW). Compared with sham operated rats, uMI rats showed a 68.5% increase in the relative contribution of V3and a 33.7% decrease in the relative contribution of V1(p < 0.05). Untreated cMI showed 39.7% more V3and 38.2% less V1when compared with untreated uMI (p < 0.05). Losartan treatment after myocardial infarction reduced the incidence of cMI from 30.4 to 4.5% and scar size from 1.52 ± 0.07 to 0.94 ± 0.11 cm2respectively. The percentage of V1in Losartan treated uMI (LuMI) was 25.2% higher than the percentage of V1in untreated uMI (p < 0.05), whereas the percentage of V3in LuMI was 24.2% lower than that in untreated uMI (p < 0.05). A positive correlation of V3myosin and scar area was observed. Our study suggests that expression of V3myosin in the left ventricle is associated with scar size and the progress of hemodynamic changes after myocardial infarction. Losartan treatment reduces scar size and wall stress of the heart after the infarct, and therefore inhibits the signals shifting myosin isoform expression from V1to V3after a myocardial infarction. |
| Databáze: |
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