Tsai Min-Shan, Sun Shijie, Tang Wanchun, Ristagno Giuseppe, Chen Wen-Jone, Weil Max Harry
Weil Institute of Critical Care Medicine, Rancho Mirage, CA, USA.
Crit Care Med. 2008 Dec;36(12):3213-9. doi: 10.1097/CCM.0b013e31818f23f0.
Previous studies demonstrated myocardial dysfunction after electrical shock and indicated it may be related to free radicals. Whether the free radicals are generated after electrical shock has not been documented at the cellular level. This study was to investigate whether electrical shock generates intracellular free radicals inside cardiomyocytes and to evaluate whether reducing intracellular free radicals by pretreatment of ascorbic acid would reduce the contractile dysfunction after electrical shock.
Randomized prospective animal study.
University affiliated research laboratory.
Sprague-Dawley rats.
Cardiomyocytes isolated from adult male rats were divided into four groups: (1) electrical shock alone; (2) electrical shock pretreated with ascorbic acid; (3) pretreated with ascorbic acid alone; and (4) control. Ascorbic acid (0.2 mM) was administrated in the perfusate of the ascorbic acid + electrical shock and ascorbic acid groups. A 2-J electrical shock was delivered to the electrical shock and ascorbic acid + electrical shock groups.
DCFH-DA-loaded cardiomyocytes showed increased intracellular free radicals after electrical shock. The contractions and Ca2+ transients were recorded optically with fura-2 loading. Within 4 mins after electrical shock in the electrical shock group, the length shortening decreased from 8.4% +/- 2.5% to 5.6% +/- 3.4% (p = 0.000) and the Ca2+ transient decreased from 1.15 +/- 0.13 au to 1.08 +/- 0.1 au (p = 0.038). Compared with control, a significant difference in length shortening (p = 0.001) but not Ca2+ transient (p = 0.052) was noted. In the presence of ascorbic acid, electrical shock did not affect length shortening and Ca2+ transient.
Electrical shock generates free radicals inside the cardiomyocyte, and causes contractile impairment and associated decrease of Ca transient. Administering ascorbic acid may improve such damage by eliminating free radicals.
以往研究表明电击后存在心肌功能障碍，并指出其可能与自由基有关。但电击后自由基是否在细胞水平产生尚未见报道。本研究旨在探讨电击是否会在心肌细胞内产生细胞内自由基，并评估通过抗坏血酸预处理减少细胞内自由基是否会减轻电击后的收缩功能障碍。
随机前瞻性动物研究。
大学附属研究实验室。
Sprague-Dawley大鼠。
从成年雄性大鼠分离的心肌细胞分为四组：（1）单纯电击组；（2）抗坏血酸预处理后电击组；（3）单纯抗坏血酸预处理组；（4）对照组。在抗坏血酸+电击组和抗坏血酸组的灌注液中加入抗坏血酸（0.2 mM）。对电击组和抗坏血酸+电击组施加2焦耳的电击。
负载DCFH-DA的心肌细胞在电击后细胞内自由基增加。用fura-2负载以光学方式记录收缩和Ca2+瞬变。在电击组电击后4分钟内，长度缩短从8.4%±2.5%降至5.6%±3.4%（p = 0.000），Ca2+瞬变从1.15±0.13 au降至1.08±0.1 au（p = 0.038）。与对照组相比，长度缩短有显著差异（p = 0.001），但Ca2+瞬变无显著差异（p = 0.052）。在存在抗坏血酸的情况下，电击不影响长度缩短和Ca2+瞬变。
电击在心肌细胞内产生自由基，导致收缩功能受损及相关的Ca瞬变减少。给予抗坏血酸可能通过清除自由基改善这种损伤。
