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首页> 外文期刊>Life sciences >LIDOCAINE DOES NOT PREVENT THE CALCIUM PARADOX IN RAT HEARTS - A LASER MICROPROBE MASS ANALYSIS (LAMMA) STUDY
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LIDOCAINE DOES NOT PREVENT THE CALCIUM PARADOX IN RAT HEARTS - A LASER MICROPROBE MASS ANALYSIS (LAMMA) STUDY

机译：利多卡因不能预防大鼠心脏中的钙过氧化物-激光微探针质量分析（LAMMA）研究

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摘要

The calcium paradox stands for the cell damage that occurs when isolated hearts are perfused with a Ca2+-free solution followed by perfusion with a Ca2+-containing solution. Although it is generally accepted that a massive Ca2+ influx during the Ca2+-repletion phase is responsible for the cell damage, there is no consensus about what makes the heart susceptible to the calcium paradox during the Ca2+-depletion phase. It has been suggested that the extent of the calcium paradox is primarily determined by accumulation of Na+ during Ca2+ depletion and a subsequent accumulation of Ca2+ via reverse Na+-Ca2+ exchange during Ca2+ repletion. According to another theory, weakening of intercalated disc junctions during Ca2+ depletion and contracture-mediated disruption of the cell membrane during Ca2+ repletion are responsible for the calcium paradox. In the present study we further investigated the possible role of Na+ in the development of the calcium paradox. During Ca2+ depletion, lidocaine was used to inhibit Na+ entry through the Na+ channels. Isolated rat hearts were perfused with Krebs Henseleit buffer (KH) containing 1.4 mM Ca2+ for 15 min, followed by 10 min of Ca2+-free perfusion and 10 min of reperfusion with Ca2+. In the treated group 0.1 mM lidocaine was present throughout the experiment. At the end of each experiment, Ca2+ cytochemistry was performed and the intracellular Ca2+ content was analyzed by laser microprobe mass analysis (LAMMA). The results show that during Ca2+ depletion, the intracellular Ca2+ content did not change significantly. Ca2+ repletion, however, gave rise to a full calcium paradox irrespective of the presence of lidocaine: massive cell damage and Ca2+ accumulation in the mitochondria. The results provide further evidence that intracellular Na+ accumulation during Ca2+ depletion is not involved in the occurrence of the calcium paradox. [References: 24]
机译：钙悖论代表的是当将离体心脏用不含Ca2 +的溶液灌注然后再灌注含Ca2 +的溶液时发生的细胞损伤。尽管人们普遍认为，在Ca2 +耗尽阶段大量的Ca2 +流入是造成细胞损伤的原因，但对于在Ca2 +耗尽阶段使心脏易患钙悖论的原因尚无共识。已经提出钙悖论的程度主要由Ca 2+耗尽期间Na +的积累和随后在Ca 2+填充期间通过反向Na + -Ca 2+交换的随后Ca 2+的积累决定。根据另一种理论，Ca 2+消耗过程中插入的椎间盘连接处的减弱和Ca 2+消耗过程中细胞膜的挛缩介导的破坏是钙悖论的原因。在本研究中，我们进一步研究了Na +在钙悖论发展中的可能作用。在Ca2 +耗尽期间，利多卡因用于抑制Na +通过Na +通道进入。用含1.4 mM Ca2 +的Krebs Henseleit缓冲液（KH）灌注离体大鼠心脏15分钟，然后进行10分钟无Ca2 +灌注和10分钟Ca2 +再灌注。在整个实验过程中，治疗组中存在0.1 mM利多卡因。在每个实验结束时，进行Ca2 +细胞化学分析，并通过激光微探针质量分析（LAMMA）分析细胞内Ca2 +含量。结果表明，在Ca2 +耗尽期间，细胞内Ca2 +含量没有明显变化。无论是否存在利多卡因，Ca2 +的补充都会引起完全的钙悖论：线粒体中大量细胞损伤和Ca2 +积累。结果提供了进一步的证据，表明在Ca2 +耗尽期间细胞内Na +的积累不参与钙悖论的发生。 [参考：24]

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