Chapter title |
Optical Action Potential Mapping in Acute Models of Ischemia–Reperfusion Injury: Probing the Arrhythmogenic Role of the Mitochondrial Translocator Protein
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Chapter number | 10 |
Book title |
Experimental Models of Cardiovascular Diseases
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Published in |
Methods in molecular biology, January 2018
|
DOI | 10.1007/978-1-4939-8597-5_10 |
Pubmed ID | |
Book ISBNs |
978-1-4939-8596-8, 978-1-4939-8597-5
|
Authors |
Zeki Ilkan, Benjamin Strauss, Chiara Campana, Fadi G. Akar, Ilkan, Zeki, Strauss, Benjamin, Campana, Chiara, Akar, Fadi G. |
Abstract |
Ischemia-reperfusion (I/R) injury causes dynamic changes in electrophysiological properties that promote the incidence of post-ischemic arrhythmias. High-resolution optical action potential mapping allows for a quantitative assessment of the electrophysiological substrate at a cellular resolution within the intact heart, which is critical for elucidation of arrhythmia mechanisms. We and others have found that pharmacological inhibition of the translocator protein (TSPO) is highly effective against postischemic arrhythmias. A major hurdle that has limited the translation of this approach to patients is the fact that available TSPO ligands have several confounding effects, including a potent negative ionotropic property. To circumvent such limitations we developed an in vivo cardiac specific TSPO gene silencing approach as an alternative. Here, we provide the methodological details of our optical action potential mapping studies that were designed to probe the effects of TSPO silencing in hearts from spontaneously hypertensive rats (SHR) that are prone to I/R injury. |
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