| ObjectiveThis study is aimed to investigate the effect of Brain Natriuretic Peptide (BNP) in heart failure rats with QT dispersion and gap junction 43 remodeling induced by pressure overload.MethodsHeart failure rats models were builded by constricting abdominal aorta and randomized to BNP group(B group), heart failure group(F group) or sham operation group(C group). The left ventricular parameter was measured by cardiac color ultrasonography 8 weeks late. B group were hypodermic injection with BNP(25 microg/kg/d, mixed with saline) for 8 weeks, F group and C group were hypodermic injection with saline for 8 weeks. Measuring ventricular electrophysiology by inserting home-made electrode into subcutaneous. Hemodynamic was observed by left common carotid artery intubation. Rat hearts were fixed with 10% formalin, embedded with paraffin and cut into slices. Observing left ventricular morphostructure by HE staining, myocardial fibrosis by Masson staining and Cx43 distribution by immunohistochemicalstaining.Results1. Hemodynamic show: MABP of F group were higher than C and B group group (P<0.05)2. Cardiac electrophysiology show: QTds of F group were longer than C and B group (P<0.05). 3. HE stain show: Cardiomyocytes of C group and B group were aligned and not hypertrophy but F group were misaligned and hypertrophy.4. Masson stain show: Myocardial fibrosis area of F group were increased than C group and B group (P<0.05)5. Immunohistochemicalstaining show: Cx43 distribution of F group were increased than C group and B group (P<0.05)ConclusionBNP can shorten QTd of heart failure Rats, increase Cx43 distribution and decrease myocardial fibrosis area in myocardium。BNP also can lower mean arterial blood pressure of heart failure Rats.The data of this study suggested that the anti-arrhythmic effects of BNP be related with the improvement of QTd, the mechanism may be enhancing the cardiac muscle gap junction communication and anti-fibrosis deposition function. |
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