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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.

circulation

In Vivo Post–Cardiac Arrest Myocardial Dysfunction Is Supported by Ca <sup>2+</sup> /Calmodulin-Dependent Protein Kinase II–Mediated Calcium Long-Term Potentiation and Mitigated by Alda-1, an Agonist of Aldehyde Dehydrogenase Type 2

In Vivo Post–Cardiac Arrest Myocardial Dysfunction Is Supported by Ca 2+ /Calmodulin-Dependent Protein Kinase II–Mediated Calcium Long-Term Potentiation and Mitigated by Alda-1, an Agonist of Aldehyde Dehydrogenase Type 2

In Vivo Post–Cardiac Arrest Myocardial Dysfunction Is Supported by Ca ²⁺ /Calmodulin-Dependent Protein Kinase II–Mediated Calcium Long-Term Potentiation and Mitigated by Alda-1, an Agonist of Aldehyde Dehydrogenase Type 2