Abstract
Ventricular dyssynchrony is characterized by a difference in timing or lack of synchrony in ventricular contraction, leading to an inefficiency of pumping blood. Ventricular dyssynchrony (VD) consists of a disruption in the normal electrical conduction system, which leads to congestive heart failure (CHF). Long‐term effects of VD that lead to CHF is well studied but little is known about the short‐term effects associated with VD. Short‐term physiological changes due to VD are crucial because electrical and mechanical abnormalities or structural changes cause a decrease in overall cardiac functionresulting in long‐term effects that may lead to CHF. Such physiological abnormalities can range from metabolic alterations, metabolic remodeling such as changes in substrate utilization, mitochondrial dysfunction, ATP deficiency, impaired contractility, and the progression of cell regeneration and cell growth, etc. Thus, theobjective of this study is to investigate short‐term cellular effects associated of induced VD in vivo. Our hypothesis is that induced left ventricular dyssynchrony (via pacing) in a non‐CHF model may lead to short‐term changes such as alterations in cardiac metabolism and mitochondrial dysfunctionresulting in structural rearrangements. Frogs will undergo ventricular pacing to induce VD. Strain patterns associated with contraction and relaxation will be analyzed to verify dyssynchrony. Paced and non‐paced regions of the heart will be analyzed to determine if reactive oxygen species (ROS) generation and mitochondrial abnormalities lead to cellular changes that may induce apoptosis leading to structural rearrangement, known as ventricular remodeling.Support or Funding InformationSupported by Cal State LA Minority Opportunities in Research MBRS‐RISE Program fund through NIH NIGMS under Grant No. R25 GM61331.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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