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首页> 美国卫生研究院文献>American Journal of Physiology - Heart and Circulatory Physiology >Hypothermia/rewarming disrupts excitation-contraction coupling in cardiomyocytes
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Hypothermia/rewarming disrupts excitation-contraction coupling in cardiomyocytes

机译：体温过低/重新武装破坏了心肌细胞的兴奋收缩耦合

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Hypothermia/rewarming (H/R) is poorly tolerated by the myocardium; however, the underlying intracellular basis of H/R-induced cardiac dysfunction remains elusive. We hypothesized that in cardiomyocytes, H/R disrupts excitation-contraction coupling by reducing myofilament Ca2+ sensitivity due to an increase in cardiac troponin I (cTnI) phosphorylation. To test this hypothesis, isolated rat cardiomyocytes (13–15 cells from 6 rats per group) were electrically stimulated to evoke both cytosolic Ca2+ ([Ca2+]cyto) and contractile (sarcomere shortening) responses that were simultaneously measured using an IonOptix system. Cardiomyocytes were divided into two groups: 1) those exposed to hypothermia (15°C for 2 h) followed by rewarming (35°C; H/R); or 2) time-matched normothermic (35°C) controls (CTL). Contractile dysfunction after H/R was indicated by reduced velocity and extent of sarcomere length (SL) shortening compared with time-matched controls. Throughout hypothermia, basal [Ca2+]cyto increased and the duration of evoked [Ca2+]cyto transients was prolonged. Phase-loop plots of [Ca2+]cyto vs. contraction were shifted rightward in cardiomyocytes during hypothermia compared with CTL, indicating a decrease in Ca2+ sensitivity. Using Western blot, we found that H/R increases cTnI phosphorylation. These results support our overall hypothesis and suggest that H/R disrupts excitation-contraction coupling of cardiomyocytes due to increased cTnI phosphorylation and reduced Ca2+ sensitivity.Listen to this article's corresponding podcast at .
机译：低温对低温/重新武装（H / R）的耐受性差；然而，H / R引起的心脏功能障碍的潜在细胞内基础仍然难以捉摸。我们假设在心肌细胞中，H / R通过降低心肌肌钙蛋白I（cTnI）磷酸化导致的肌丝Ca 2 + 敏感性来破坏兴奋收缩耦合。为了验证这一假设，对电离的大鼠心肌细胞（每组6只大鼠的13-15个细胞）进行电刺激，以唤起两种胞质Ca 2 + （[Ca 2 + ]细胞）和收缩（肌节缩短）反应，同时使用IonOptix系统进行了测量。心肌细胞分为两组：1）暴露于低温（15°C 2 h），然后再加热（35°C; H / R）的细胞；或2）时间匹配的常温（35°C）对照（CTL）。与时间匹配的对照组相比，H / R后的收缩功能障碍通过降低的速度和肌节长度（SL）缩短的程度来表明。在整个低温过程中，基础[Ca 2 + ]细胞增加，诱发的[Ca 2 + ]细胞瞬变持续时间延长。与CTL相比，低温期间心肌细胞中[Ca 2 + ]细胞与收缩的相环图向右移动，表明Ca 2 + 敏感性降低。使用蛋白质印迹，我们发现H / R增加cTnI磷酸化。这些结果支持了我们的整体假设，并表明H / R会由于cTnI磷酸化的增加和Ca 2 + 的敏感性降低而中断心肌细胞的兴奋-收缩偶联。

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