| Autor: |
Welsh DC; Cardiovascular Research Group, Temple University Medical Center, Philadelphia, Pennsylvania 19140, USA., Dipla K, McNulty PH, Mu A, Ojamaa KM, Klein I, Houser SR, Margulies KB |
| Jazyk: |
angličtina |
| Zdroj: |
American journal of physiology. Heart and circulatory physiology [Am J Physiol Heart Circ Physiol] 2001 Sep; Vol. 281 (3), pp. H1131-6. |
| DOI: |
10.1152/ajpheart.2001.281.3.H1131 |
| Abstrakt: |
The present study was designed to determine whether myocardial atrophy is necessarily associated with changes in cardiac contractility. Myocardial unloading of normal hearts was produced via heterotopic transplantation in rats. Contractions of isolated myocytes (1.2 mM Ca2+; 37 degrees C) were assessed during field stimulation (0.5, 1.0, and 2.0 Hz), and papillary muscle contractions were assessed during direct stimulation (2.0 mM Ca2+; 37 degrees C; 0.5 Hz). Hemodynamic unloading was associated with a 41% decrease in median myocyte volume and proportional decreases in myocyte length and width. Nevertheless, atrophic myocytes had normal fractional shortening, time to peak contraction, and relaxation times. Despite decreases in absolute maximal force generation (F(max)), there were no differences in F(max)/ area in papillary muscles isolated from unloaded transplanted hearts. Therefore, atrophic remodeling after unloading is associated with intact contractile function in isolated myocytes and papillary muscles when contractile indexes are normalized to account for reductions in cell length and cross-sectional area, respectively. Nevertheless, in the absence of compensatory increases in contractile function, reductions in myocardial mass will lead to impaired overall work capacity. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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