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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:体内心脏骤停后心肌功能障碍由Ca2 + /钙调蛋白依赖性蛋白激酶II介导的钙长期增强和Alda-1(醛脱氢酶2型激动剂)缓解。

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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:心脏骤停后的生存受到逮捕后心肌功能障碍的限制,但是由于缺乏疾病生理模型的数据,对这种现象的理解受到了限制。在这项研究中,我们建立了心脏骤停和复苏的体内模型,描述了相关心肌功能障碍的生物学特征,并测试了新的治疗策略。

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