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首页> 外文期刊>Circulation: An Official Journal of the American Heart Association >In Vivo Post-Cardiac Arrest Myocardial Dysfunction Is Supported by Ca2+/Calmodulin-Dependent Protein Kinase II-Mediated Calcium Long-Term Potentiation and Mitigated by Alda-1, an Agonist of Aldehyde Dehydrogenase Type 2
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In Vivo Post-Cardiac Arrest Myocardial Dysfunction Is Supported by Ca2+/Calmodulin-Dependent Protein Kinase II-Mediated Calcium Long-Term Potentiation and Mitigated by Alda-1, an Agonist of Aldehyde Dehydrogenase Type 2

机译:在体内心脏病后骤停心肌功能障碍得到CA2 + /钙调蛋白依赖性蛋白激酶II介导的长期增强,并通过ALDA-1减轻醛脱氢酶2型的激动剂

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摘要

BACKGROUND: Survival after sudden cardiac arrest is limited by postarrest myocardial dysfunction, but understanding of this phenomenon is constrained by a lack of data from a physiological model of disease. In this study, we established an in vivo model of cardiac arrest and resuscitation, characterized the biology of the associated myocardial dysfunction, and tested novel therapeutic strategies.
机译:背景:突然心脏骤停后生存受到后藻露的心肌功能障碍的限制,但了解这种现象受到疾病生理模型的缺乏数据的限制。 在这项研究中,我们建立了体内心脏骤停和复苏模型,其特征在于相关心肌功能障碍的生物学,并测试了新的治疗策略。

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