Reduced Sensory Nerve Fiber Density in Ventricular Myocardium in a Rat Myocardial Infarction Heart Failure Model

Abstract

IntroductionHeart failure (HF) results in autonomic dysfunction, characterized by sympathetic activation and vagal withdrawal, which in turn contributes to HF progression. The cardiac afferent sensory nerves play a critical role in mediating cardiovascular reflexes and in the neural regulation of cardiovascular function. However, the role of cardiac sensory nerves in mediating autonomic dysfunction in HF is less studied and it is unknown whether HF causes cardiac sensory nerve remodeling.MethodsMyocardial infarction (MI) was induced by left anterior coronary artery ligation in 9 rats, with 8 sham‐operated animals serving as controls. Two months after MI surgery, HF was confirmed in post‐MI rats (MI‐HF) by echocardiography and hemodynamic measurements. Sensory nerve fibers in ventricular myocardium were visualized on frozen histological sections by immunostaining with anti‐calcitonin gene related peptide (CGRP) antibody. The density of CGRP‐positive nerve fibers was determined on digitized images of non‐infarcted ventricular myocardium (remote from the infarction area) by using Image‐Pro Analyzer v.7.0 software.ResultsCompared to controls, the sensory nerve fiber density in non‐infarcted ventricular myocardium was significantly decreased in MI‐HF animals (see figure).ConclusionsThe development of HF in post‐MI rats is associated with a significant sensory nerve fiber remodeling with reduced sensory nerve fiber density.