Optogenetic Pacing and Defibrillation

The expression of the light gated ion channel channelrhodopsin2 (ChR2) in cardiomyocytes of mouse hearts enables optogenetic pacing as well as defibrillation to terminate ventricular tachycardia by epicardial illumination with a novel mechanism of endocardial conduction block. Therefore, light transmission, epi- to endocardial cell coupling and the extent of light-induced transmural depolarization are important parameters to predict the effectiveness of optogenetic pacing and defibrillation in hearts larger than mouse hearts.

In this project, we investigate light transmission of myocardial tissue and the influence of blood at defined wavelengths from 350 to 800 nm. Furthermore, we measure depolarization of resting membrane potential by epicardial illumination at calibrated depths in the ventricular wall to estimate electrical coupling. Although light is attenuated at deeper layers, the electrical coupling from above increases depolarization and thereby helps conduction block for successful defibrillation.