Objective: To explore the remodeling mechanism of myocardium and sympathetic nerve in pressure overload left ventricular hypertrophy and elucidate the protective effect of statins.
Methods: Pressure-overload left ventricular hypertrophy (LVH) of rats was induced by partial coarctation of abdominal aorta; a sham-operated group served as the control (SHAM, n = 22). At 8 weeks post-operation, the animals were divided into two groups and a 12-week treatment period was investigated. At the end of treatment period, echocardiographic evaluations and hemodynamic measurements were performed. Sympathetic innervation was investigated by analyzing nerve growth factor (NGF), growth associated protein-43 (GAP43) and tyrosine hydroxylase (TH).
Results: In LVH rats, a significant increase of left ventricular weight, left ventricular weight/body weight, echocardiographic left ventricular end-diastolic diameter, interventricular septum thickness, posterior left ventricular wall thickness, left ventricular systolic pressure and dP/dt was observed. The expressions of NGF and GAP43 protein were significantly down-regulated (0.82 +/- 0.06 vs 1.53 +/- 0.10, 0.68 +/- 0.06 vs 0.81 +/- 0.10) and TH level was up-regulated (0.44 +/- 0.10 vs 0.62 +/- 0.06) by RSV treatment.
Conclusion: A HMG CoA inhibitor reverses the development of left ventricular hypertrophy and inhibits sympathetic innervation in abdominal aortic-clamped animals.