Abstract
To assess the effect of nesiritide on the endothelial function of iliac arteries following endothelia trauma. Right iliac artery trauma was created with a balloon catheter. Ten rabbits were treated with a 4-week subcutaneous injection of nesiritide at a fixed daily dose of 0.1mg/kg. Ten rabbits received daily normal saline injection. Plasma endothelin 1 (ET-1), nitric oxide (NO), and Von Willebrand Factor (vWF) were measured before and after the therapies. Tissue proliferating cell nuclear antigen (PCNA) was measured after the treatment. After the treatment, in the therapeutic group, the area under internal elastic membrane and the residual lumen area were higher than in the normal saline group (P <0.05). The plasma levels of ET-1 (91.6±6.8 vs 114.9±6.3 ng/L, P =0.001), vWF (134.6±10.8% vs 188.8±10.4%, P =0.001) and the ratio of PCNA positive expression (11.7±4.2% vs 36.2±11.4%, P =0.005) in the therapeutic group was lower than in the normal saline group, while the plasma levels of NO was higher (89.7±9.3 vs 43.5±5.3 µmol/L, P =0.001). Nesiritide inhibited remodeling of rabbit iliac artery following endothelial trauma. The inhibition of vascular remodeling may be related to the alleviated endothelial dysfunction and reduced expression of tissue proliferating cell nuclear antigen.
Highlights
The B-type natriuretic peptide (BNP) is a vasoactive peptide
We investigated the changes in plasma endothelin 1 (ET-1), nitric oxide (NO), Von Willebrand Factor (vWF) and neointimal proliferation following nesiritide therapy in a rabbit model that we have previously reported (Liu et al, 2010, 2012)
The two remodeling measures (AUIEM and residual lumen areas) in the control animals were lower than the therapeutic group animals (P =0.025 and P =0.001, respectively, Table I), whereas the stenosis ratio in the study group was higher (P =0.001, Table I)
Summary
The B-type natriuretic peptide (BNP) is a vasoactive peptide. After more than two decades of active investigations, BNP has become a useful biomarker for the diagnosis of congestive heart failure and risk stratification of this prevalent and chronic condition (Egom, 2015; We et al 2005a, 2005b, 2005c; Sun et al, 2007). BNP exerts protective effects against the post-myocardial infarction remodeling processes. BNP treatment inhibits extracellular matrix remodeling following acute myocardial.
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