Salvia miltiorrhiza attenuates the changes in contraction and intracellular calcium induced by anoxia and reoxygenation in rat cardiomyocytes

The aim of the present study is to investigate the effect of Salvia miltiorrhiza (SM) on contraction and the intracellular calcium of isolated ventricular myocytes during normoxia or anoxia and reoxygenation using a video tracking system and spectrofluorometry. Cardiac ventricular myocytes were isol...

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Published inLife sciences (1973) Vol. 72; no. 22; pp. 2451 - 2463
Main Authors Cao, Chun-Mei, Xia, Qiang, Zhang, Xiong, Xu, Wan-Hong, Jiang, Hui-Di, Chen, Jun-Zhu
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier Inc 18.04.2003
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Summary:The aim of the present study is to investigate the effect of Salvia miltiorrhiza (SM) on contraction and the intracellular calcium of isolated ventricular myocytes during normoxia or anoxia and reoxygenation using a video tracking system and spectrofluorometry. Cardiac ventricular myocytes were isolated enzymatically by collagenase and exposed to 5 min of anoxia followed by 10 min of reoxygenation. SM (1–9 g/L) depressed both contraction and the [Ca2+]i transient in a dose-dependent manner. SM did not affect the diastolic calcium level and the sarcolemmal Ca2+ channel of myocytes but decreased the caffeine-induced calcium release. During anoxia, the ±dL/dtmax, amplitudes of contraction (dL) of cell contraction and [Ca2+]i transients were decreased, while the diastolic calcium level was increased. None of the parameters returned to the pre-anoxia level during reoxygenaton. However, SM (3 g/L) did attenuate the changes in cell contraction and intracellular calcium induced by anoxia and reoxygenation. It is concluded that SM has different effects on normoxic and anoxic cardiomyocytes. The SM-induced reduction of changes in contraction and intracellular calcium induced by anoxia/reoxygenation indicates that SM may be beneficial for cardiac tissue in recovery of mechanical function and intracellular calcium homeostasis.
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ISSN:0024-3205
1879-0631
DOI:10.1016/S0024-3205(03)00142-5