2007Chinese Journal of ArteriosclerosisRequires access

Effects of Metoprolol Treatment on Neural Remodeling After Myocardial Infarction in Rabbits

Hu He

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Abstract

Aim To investigate the influence of β-blocker (metoprolol) on the ventricular neural remodeling and susceptibility to ventricular arrhythmias. Methods New Zealand rabbits were ligated with left anterior descending branch for myocardial infarction (MI) induction. The rabbits were randomized to metoprolol group treated with metoprolol [10 mg/(kg·d)], MI group and sham operation group. All groups were further followed up for 8 weeks. After electrophysiological recordings, immunostaining was applied to detect the shape and density of nerve fibers. Results Eight weeks after operation, metoprolol treatment reduced the increased incidence of post-MI ventricular arrhythmias compared with those placebo treatment (8.3% vs 58.3%, P0.001). The densities of S100 and GAP43 positive nerve fibers (3 889±521 μm2/mm2, 3 090±622 μm2/mm2) were significantly higher in MI group than in sham operation group (1 727±304 μm2/mm2,718±177 μm2/mm2)at infarct border. Additionally, the distribution of nerve fibers in the MI group were obviously diverse in contrast to sham group. The densities of S100 and GAP43 positive nerve fibers dropped to 2 725±283 μm2/mm2 and 1 922±508 μm2/mm2 at infarct border after meteprolol treatment. Otherwise, metoprolol attenuated the heterogeneity of cardiac innervation. The densities of S100 and GAP43 positive nerve fibers at non-infarct left ventricular free wall were also lowered by meteprolol treatment in MI model. Conclusion Metoprolol appeared to reduce the post-MI ventricular arrhythmias, partly by improving neural remodeling.

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Aim To investigate the influence of β-blocker (metoprolol) on the ventricular neural remodeling and susceptibility to ventricular arrhythmias. Methods New Zealand rabbits were ligated with left anterior descending branch for myocardial infarction (MI) induction. The rabbits were randomized to metoprolol group treated with metoprolol [10 mg/(kg·d)], MI group and sham operation group. All groups were further followed up for 8 weeks. After electrophysiological recordings, immunostaining was applied to detect the shape and density of nerve fibers. Results Eight weeks after operation, metoprolol treatment reduced the increased incidence of post-MI ventricular arrhythmias compared with those placebo treatment (8.3% vs 58.3%, P0.001). The densities of S100 and GAP43 positive nerve fibers (3 889±521 μm2/mm2, 3 090±622 μm2/mm2) were significantly higher in MI group than in sham operation group (1 727±304 μm2/mm2,718±177 μm2/mm2)at infarct border. Additionally, the distribution of nerve fibers in the MI group were obviously diverse in contrast to sham group. The densities of S100 and GAP43 positive nerve fibers dropped to 2 725±283 μm2/mm2 and 1 922±508 μm2/mm2 at infarct border after meteprolol treatment. Otherwise, metoprolol attenuated the heterogeneity of cardiac innervation. The densities of S100 and GAP43 positive nerve fibers at non-infarct left ventricular free wall were also lowered by meteprolol treatment in MI model. Conclusion Metoprolol appeared to reduce the post-MI ventricular arrhythmias, partly by improving neural remodeling.

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Available abstract

Aim To investigate the influence of β-blocker (metoprolol) on the ventricular neural remodeling and susceptibility to ventricular arrhythmias. Methods New Zealand rabbits were ligated with left anterior descending branch for myocardial infarction (MI) induction. The rabbits were randomized to metoprolol group treated with metoprolol [10 mg/(kg·d)], MI group and sham operation group. All groups were further followed up for 8 weeks. After electrophysiological recordings, immunostaining was applied to detect the shape and density of nerve fibers. Results Eight weeks after operation, metoprolol treatment reduced the increased incidence of post-MI ventricular arrhythmias compared with those placebo treatment (8.3% vs 58.3%, P0.001). The densities of S100 and GAP43 positive nerve fibers (3 889±521 μm2/mm2, 3 090±622 μm2/mm2) were significantly higher in MI group than in sham operation group (1 727±304 μm2/mm2,718±177 μm2/mm2)at infarct border. Additionally, the distribution of nerve fibers in the MI group were obviously diverse in contrast to sham group. The densities of S100 and GAP43 positive nerve fibers dropped to 2 725±283 μm2/mm2 and 1 922±508 μm2/mm2 at infarct border after meteprolol treatment. Otherwise, metoprolol attenuated the heterogeneity of cardiac innervation. The densities of S100 and GAP43 positive nerve fibers at non-infarct left ventricular free wall were also lowered by meteprolol treatment in MI model. Conclusion Metoprolol appeared to reduce the post-MI ventricular arrhythmias, partly by improving neural remodeling.

Key concepts: Metoprolol, Medicine, Cardiology, Ventricular remodeling, Myocardial infarction, Internal medicine, Gap-43 protein, Infarction

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