Increased calcium loading and inotropy without greater cell death in hypoxic rat cardiomyocytes.
Increased calcium loading and inotropy without greater cell death in hypoxic rat cardiomyocytes.
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缺氧大鼠心肌细胞中钙负荷和正性肌力增加，且细胞死亡不增加。
DOI：
10.1152/ajpheart.1998.275.6.h2272
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发表时间：
1998
期刊：
影响因子：
--
通讯作者：
Suter,TM
中科院分区：
文献类型：
--
作者：
Kondo,RP;Apstein,CS;Eberli,FR;Tillotson,DL;Suter,TM
为了测试用高葡萄糖（19.5mM）处理的“缺氧”肌细胞中的收缩功能是否可以通过增加细胞内Ca 2+而不加速细胞挛缩或死亡来改善，我们用高细胞外Ca 2+浓度（[Ca 2 +]o）挑战代谢抑制的起搏肌细胞，并同时测量细胞缩短和细胞内Ca 2+浓度（[Ca 2 +]i）。生理[Ca 2 +]水平（1.2 mM）的NaCN暴露导致收缩功能下降至NaCN前值的58 ± 8%（P< 0.001），但收缩和舒张[Ca 2 +] i分别比基线增加104 ± 17和37 ± 9%（P< 0.01）。在NaCN存在的情况下，[Ca 2 +] o2.4 mM的浓度倍增，立即恢复收缩功能，18 min后的抽搐幅度为123 ± 14%（P< 0.001）基线前NaCN值，而收缩期[Ca ~（2+）] i进一步升高至基线的225 ± 63%（P< 0.05），舒张期[Ca ~（2+）] i升高至基线的73 ± 16%（P< 0.01）。这种[Ca ~（2+）] i的显著增加对心肌细胞舒张功能或存活率没有有害影响。这些结果表明，如果提供足够的代谢底物，在代谢抑制，缺氧心肌细胞的收缩功能可以通过增加[Ca ~（2+）] i而不引起短期细胞损伤。
To test whether contractile function in “hypoxic” myocytes treated with high glucose (19.5 mM) can be improved by increasing intracellular Ca2+without accelerating cell contracture or death, we challenged metabolically inhibited, paced myocytes with high extracellular Ca2+concentration ([Ca2+]o) and measured simultaneously cell shortening and intracellular Ca2+concentration ([Ca2+]i). NaCN exposure at a physiological [Ca2+]olevel (1.2 mM) caused a decline of contractile function to 58 ± 8% of the pre-NaCN value (P< 0.001) but increased systolic and diastolic [Ca2+]iby 104 ± 17 and 37 ± 9% above baseline (P< 0.01), respectively. Consequent doubling of [Ca2+]oto 2.4 mM, in the presence of NaCN, immediately restored contractile function, and twitch amplitude after 18 min was 123 ± 14% (P< 0.001) of baseline pre-NaCN values, whereas systolic [Ca2+]iincreased further to 225 ± 63% (P< 0.05) and diastolic [Ca2+]ito 73 ± 16% above baseline (P< 0.01). This marked increase in [Ca2+]ihad no deleterious effect on myocyte diastolic function or survival. These results suggest that if adequate metabolic substrate is provided, contractile function in metabolically inhibited, hypoxic myocytes can be restored by increasing [Ca2+]iwithout causing short-term cell injury.