| Autor: |
DAVIDOFF, A W, BOYDEN, P A, SCHWARTZ, K, MICHEL, J B, ZHANG, Y M, OBAYASHI, M, CRABBE, D, KEURS, H E D J |
| Předmět: |
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| Zdroj: |
Annals of the New York Academy of Sciences; 2004, Vol. 1015 Issue 1, p84-95, 12p |
| Abstrakt: |
The causes of reduced cardiac force development in congestive heart failure (CHF) are still uncertain. We explored the subcellular mechanisms leading to decreased force development in trabeculae from rats with a myocardial infarction. We defined CHF according to clinical and pathological criteria and compared properties of trabeculae from animals with CHF (cMI) to those of animals with a myocardial scar but without evidence of CHF (uMI), and sham-operated animals. The new findings of this study on properties of cMI trabeculae are that (1) maximal twitch force following post-extrasystolic potentiation is unchanged; (2) the sensitivity of cMI trabeculae to [Ca2+]o is in- creased; (3) spontaneous diastolic sarcomere length (SL) fluctuations (SA) are increased in cMI at all levels of SR Ca2+ loading; and (4) SA is accompanied by a proportional reduction of Fmax. The results suggest that the probability of spontaneous diastolic opening of SR Ca2+ channels is increased in CHF. These data provide the basis for a novel mechanism underlying systolic and diastolic dysfunction as well as arrhythmias in hearts in CHF. If SA proves to be a component of myocardial dysfunction in human CHF, our thinking about therapy of the patient with CHF may be profoundly changed. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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