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ULTRASOUND-INDUCED CHANGES IN DEPOLARIZATION OF NEONATAL VENTRICULAR CARDIOMYOCYTES
Poster   Open access   Peer reviewed

ULTRASOUND-INDUCED CHANGES IN DEPOLARIZATION OF NEONATAL VENTRICULAR CARDIOMYOCYTES

Natasha Mehta, Randall Lee, Youhan Sunny, Chris Bawiec, Steven Kutalek, Peter Lewin and Andrew Kohut
Journal of the American College of Cardiology, v 65(10), A495
17 Mar 2015
DOI: https://doi.org/10.1016/S0735-1097(15)60495-8
url
https://doi.org/10.1016/s0735-1097(15)60495-8View
Published, Version of Record (VoR)Maybe Open Access (Publisher Bronze),  Open

Abstract

Cardiomyocytes Rodents Ultrasonic imaging
Background: Ultrasound interacts 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 on microelectrode arrays to record action potentials (AP) and analyze depolarization patterns. A custom 2.5 MHz unfocused ultrasound transducer was directed at 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. Multiple trials were conducted at each setting with 30 total trials; consisting of 30s continuous ultrasound exposure with subsequent off interval of 1 minute. Results: AP durations, peak amplitudes, including peak maximum and minimum were analyzed pre and post-ultrasound exposure on consecutive days. AP durations in both groups remained consistent averaging 30-50ms. Interestingly, peak maximum and minimum AP amplitudes, which initially ranged from 20-30mV, nearly doubled with ultrasound exposure. This increase in peak amplitude was more prominent after several days of repeated ultrasound exposure. In addition, new small APs were observed before or after large APs post-ultrasound with an increasingly distinct pattern on subsequent days. Conclusion: Our trials consistently demonstrated the ability of ultrasound energy to not only perpetuate APs but also induce new depolarizations with successive exposure to ultrasound over consecutive days without compromising AP duration. These manifestations may be the result of ultrasound energy conditioning [Na+] and [Ca+2] ion channels responsible for cardiac depolarization. It can also be theorized that ultrasound energy induces more pacemaker activity by mechanically stimulating cells or by increasing ion currents within the cells.

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Web of Science research areas
Cardiac & Cardiovascular Systems
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