A theoretic model for sonogenetic antiarrhythmia

TL;DR

This paper develops a quantitative model linking ultrasonic radiation force to ion channel activation in cardiac cells, proposing a sonogenetic approach for noninvasive arrhythmia treatment.

Contribution

It introduces a novel quantitative model connecting ultrasonic radiation force to membrane tension and ion channel regulation in cardiomyocytes for arrhythmia therapy.

Findings

Model predicts ion channel opening probability under ultrasonic force

Sonogenetic mechanism can potentially eliminate arrhythmias

Provides a theoretical basis for noninvasive arrhythmia treatment

Abstract

Sonogenetics can be used as a new alternative for treating arrhythmia due to its advantages of noninvasive, high safety and strong penetration. In the treatment of arrhythmias by sonogenetics, cardiac myocytes are deformed by ultrasonic radiation force. We quantitatively calculated the shape variation of cardiomyocytes under ultrasonic radiation force, and the deformation of cardiomyocytes caused the change of membrane tension. Membrane tension consists of two parts, plasma membrane tension and cortical tension between the cell membrane and cytoskeleton. Since plasma membrane tension was mainly considered in existing experiments, we proposed a quantitative model of the relationship between ultrasonic radiation force and plasma membrane tension. The Boltzmann relationship between plasma membrane tension and ion channel opening probability is presented based on the experimental results of ion channel activation by stretching. Finally, a quantitative model was obtained for ultrasonic radiation force to regulate the opening probability of ion channel activated by stretching. Based on this quantitative model, we proposed the regulation mechanism of ultrasonic radiation force under hypercompression and hyperstretching, and verified that this mechanism can eliminate arrhythmias by sonogenetics.