The neural remodeling of the atrium plays an important role in the initiation of atrial fibrillation after myocardial infarction (MI); however, the effects of the left stellate ganglion (LSG) on the neural remodeling of the atrium remain incompletely understood. Thus, this study investigated the mechanism by which the LSG mediates sympathetic neural remodeling of the left atrium (LA) in rats after MI.Methods:
Sixty rats were randomly divided into a Sham group and an MI group. The expression levels of growth-associated protein-43 (GAP43) and nerve growth factor (NGF) messenger ribonucleic acid (mRNA) were measured by reverse transcription polymerase chain reaction. Immunohistochemistry was used to detect the distribution and density of GAP43- and NGF-positive nerves. The expression levels of the proteins were quantified by Western blotting.Results:
Compared with the Sham group, GAP43 mRNA expression in the LSG was increased in the MI group (P < 0.01), but not significantly increased in the LA. Immunohistochemical analysis demonstrated that in both the LSG and the LA, the mean densities of GAP43- and NGF-positive nerves in the MI group were increased (P < 0.01). In both the LSG and the LA, the protein levels of GAP43 and NGF in the MI group were increased relative to the Sham group (P < 0.01).Conclusions:
The increased levels of NGF and GAP43 proteins can induce sympathetic nerve hyperinnervation in the LSG and the LA after MI. The increased GAP43 proteins in the LA, which may have been transported from the LSG, accelerated LA sympathetic neural remodeling in rats.