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Updated: Jul 16, 2026

Permanent Ligation of the Left Anterior Descending Coronary Artery in Mice: A Model of Post-myocardial Infarction Remodelling and Heart Failure
Published on: December 2, 2014
Relationship between sympathetic nerve sprouting and repolarization dispersion at peri-infarct zone after myocardial
Hong Jiang1, Zhibing Lu, Ying Yu
1Department of Cardiology, Renming hospital of Wuhan University, 238 Jiefang Road, Wuchang, Wuhan 430060, China. hong_j_wurm@163.com
Abstract:
Sympathetic nerve sprouting is thought to contribute to sudden cardiac death (SCD) in chronic myocardial infarction (MI). However, the mechanisms remain unclear. This study investigated the relationship between sympathetic nerve sprouting and repolarization dispersion at peri-infarct zones after MI. Thirty adult New Zealand White rabbits underwent coronary artery ligation (MI group: n=20) or sham operation (SO group: n=10). Eight weeks after surgery, transmural dispersion of repolarization (TDR) was examined at the peri-infarct zones in MI group and corresponding zones in the SO group at baseline and during sympathetic nerve stimulation. Sympathetic nerve sprouting was detected by immunocytochemical staining using anti-growth associated protein 43 (GAP43) and anti-tyrosine hydroxylase (TH) antibodies. The results demonstrated that TDR was significantly larger at peri-infarct zones in MI group than the corresponding zone in SO group at baseline or during sympathetic nerve stimulation. The densities of both GAP43- and TH-positive nerves were significantly higher at peri-infarct zones in infracted hearts than the corresponding zones in control hearts (both p<0.01). In the MI group, the density of GAP43- or TH-positive nerves at peri-infarct zones had a significantly positive correlation with the TDR or DeltaTDR (change in TDR) at baseline as well as with sympathetic nerve stimulation (p<0.05 for all). These results suggested that sympathetic nerve sprouting is more pronounced and heterogeneous at peri-infarct zones at 8 weeks after MI. The excessive sprouting of sympathetic nerves increases local ventricular TDR, which may be a potential mechanism for SCD in chronic MI.
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