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Ultrasound-Induced Inhibition and Modulation of Neonatal Ventricular Cardiomyocyte Depolarization
Abstract   Peer reviewed

Ultrasound-Induced Inhibition and Modulation of Neonatal Ventricular Cardiomyocyte Depolarization

Natasha Mehta, J Yasha Kresh, Steven P Kutalek, Peter A Lewin and Andrew R Kohut
Circulation research, v 115(suppl_1), A158
18 Jul 2014
DOI: https://doi.org/10.1161/res.115.suppl_1.158

Abstract

Background: Ultrasound can interact with tissue through either thermal or non-thermal physical mechanisms. Radiation force has been shown to stimulate cardiac and neural tissue in vivo. Ultrasound might hold clinical potential as a noninvasive therapeutic tool via specific bioeffects on cardiomyocytes. This study aims to assess the effect of ultrasound on cardiomyocyte depolarization in a tissue culture model. Methods: Cardiomyocytes were isolated from neonatal rat ventricular tissue and plated directly on microelectrode arrays to record depolarization patterns. A custom 2.5 MHz unfocused ultrasound transducer was directed at the cardiomyocytes in a tissue culture model. A function generator, with an amplified signal +50 dB, delivered acoustic energy at variable settings of 0.1, 0.3, 0.5 and 1.0 Vpp, pulse durations of 2, 5 and 10 ms, and burst periods of 100, 250 and 300 ms. Five trials were conducted at each setting (36 total trials) with 30s of continuous ultrasound exposure followed by an off interval of 1 minute. Results: The R-R interval durations (ID) were measured throughout the recording period. Prior to ultrasound delivery, the IDs were highly irregular, ID range = 0.3-2.7 s. As ultrasound was delivered in an asynchronous manner, using 0.1 and 0.3 Vpp and PD = 2 and 5 ms, there was suppression/inhibition of cellular depolarization for the first 5-10 s. Then 10-15 s after the start of ultrasound delivery, the depolarization rate increased and demonstrated less R-R interval variability (ID=0.88-1.03 s, P value<0.05), even after the ultrasound exposure. Conclusion: Ultrasound can inhibit and modify the frequency of spontaneous electrical depolarizations of neonatal ventricular cardiomyocytes in a tissue culture model. Our observations could be due to conditioning via stretch and compression-mediated mechanosensitive pathways, by modifying intracellular calcium handling or altering cell signaling.

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