Changes in calcium handling in atrophic heterotopically isotransplanted rat hearts
Jazyk angličtina Země Německo Médium print
Typ dokumentu srovnávací studie, časopisecké články, práce podpořená grantem
PubMed
8967890
DOI
10.1007/bf00788540
Knihovny.cz E-zdroje
- MeSH
- atrofie metabolismus patologie patofyziologie MeSH
- heterotopická transplantace MeSH
- krysa rodu Rattus MeSH
- srdeční komory metabolismus patologie patofyziologie MeSH
- transplantace srdce fyziologie MeSH
- vápník metabolismus MeSH
- velikost orgánu MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- srovnávací studie MeSH
- Názvy látek
- vápník MeSH
Atrophy of the rat heart induced by hemodynamic unloading after heterotopic transplantation is associated with impaired relaxation while systolic function remains normal when compared to the heart of the recipient animal. To identify possible underlying mechanisms for the above, we studied some aspects of membrane calcium handling using postextrasystolic potentiation of contractions in the isolated right ventricular papillary muscle and in the left ventricle of the Langendorff-perfused heart. We also compared the alterations of the unloaded heart with those of overloaded hypertrophic hearts of rats with suprarenal aortic constriction. In the atrophic heart the degree of potentiation after one extrasystole, considered to be proportional to the trans-sarcolemmal influx of Ca2+ during an action potential, was increased by 125% when compared with recipient hearts. The rate of decay of potentiation which reflects the fraction of activator Ca2+ recirculating in the cells via the sarcoplasmic reticulum, negatively correlated with the degree of potentiation, although its mean value was not significantly altered. In hypertrophic hearts the decay of potentiation was faster when compared with the hearts of sham-operated animals, indicating a decreased recirculating fraction of Ca2+ The data suggest that the relative importance of trans-sarcolemmal Ca2+ fluxes is increased both in cardiac atrophy and hypertrophy; but their quantitative role in the control of cardiac contraction might differ.
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Sixty Years of Heart Research in the Institute of Physiology of the Czech Academy of Sciences
