@article{APS9454,
author = {Chun-kai HUANG and Bi-yi CHEN and Ang GUO and Rong CHEN and Yan-qi ZHU and William KUTSCHKE and Jiang HONG and Long-sheng SONG},
title = {Sildenafil ameliorates left ventricular T-tubule remodeling in a pressure overload-induced murine heart failure model},
journal = {Acta Pharmacologica Sinica},
volume = {37},
number = {4},
year = {2017},
keywords = {},
abstract = {Aim:Sildenafil, a phosphodiesterase 5 (PDE5) inhibitor, has been shown to exert beneficial effects in heart failure. The purpose of this study was to test whether sildenafil suppressed transverse-tubule (T-tubule) remodeling in left ventricular (LV) failure and thereby providing the therapeutic benefits.
Methods: A pressure overload-induced murine heart failure model was established in mice by thoracic aortic banding (TAB). One day after TAB, the mice received sildenafil (100 mg·kg-1·d-1, sc) or saline for 5 weeks. At the end of treatment, echocardiography was used to examine LV function. Then the intact hearts were dissected out and placed in Langendorff-perfusion chamber for in situ confocal imaging of T-tubule ultrastructure from epicardial myocytes.
Results: TAB surgery resulted in heart failure accompanied by remarkable T-tubule remodeling. Sildenafil treatment significantly attenuated TAB-induced cardiac hypertrophy and congestive heart failure, improved LV contractile function, and preserved T-tubule integrity in LV cardiomyocytes. But sildenafil treatment did not significantly affect the chamber dilation. The integrity of LV T-tubule structure was correlated with cardiac hypertrophy (R2=0.74, P},
issn = {1745-7254}, url = {http://www.chinaphar.com/article/view/9454}
}