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Effect of Valsartan on Pulmonary Artery Smooth Muscle Cell Hyperplasia in Rats

Author: FengZanXiang
Tutor: MaoZhiFu
School: Wuhan University
Course: Surgery
Keywords: Proliferate Smooth muscle cells Pulmonary hypertension Valsartan Treatment
CLC: R96
Type: Master's thesis
Year: 2005
Downloads: 37
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Abstract

The left-right shunt heart disease with pulmonary hypertension flag condition has entered a serious stage. Renin - angiotensin - aldosterone system (RAAS) activation and high expression is one of the main contributing factor in the development of pulmonary hypertension. Clinical treatment of pulmonary hypertension lot, but the effect is less than ideal. Investigated the effects of angiotensin - II receptor antagonist valsartan buck and pulmonary hypertension in rats pulmonary vascular smooth muscle cell proliferation and designed to help provide for the treatment of pulmonary hypertension patients. In this study the 6 to 7-week-old male Wistar rats 48 (weighing 180 to 200 g) were randomly divided into six groups: 6 weeks the control group (Ⅰ group, n = 8), 6-week shunt group (II group, n = 8), 6 weeks of treatment group (group Ⅲ, n = 8), 11 weeks the control group (IV group, n = 8), 11-week shunt group (Ⅴ group, n = 8) and 11 weeks of treatment group (Ⅵ group , n = 8). Triage and treatment groups with reference Qi Jianguang Law abdominal aorta - the inferior vena cava gastrostomy establish a left-to-right shunt pulmonary hypertension animal model, treatment group ^{to valsartan (40 mg · kg -1 · d ^{-1 ) by gavage. 6 weeks of feeding, after 11 weeks, mean pulmonary arterial pressure (PAMP) right heart catheterization. The animals were sacrificed specimens were taken to the determination and calculation of the degree of right ventricle / left ventricle, interventricular septum (RV / LV S) reflect right ventricular hypertrophy degrees, measured and calculated lung tissue (left lung) dry weight / wet weight percentages reflect pulmonary interstitial hyperplasia. Along the hilum into the boundary line is drawn, the conventional HE and mouse anti-rat antibody staining of proliferating cell nuclear antigen (PCNA). Light microscope slice, the application CMIAS image processing and analysis system calculated the muscular artery of the lung medium-sized and small muscular arteries relative medial thickness (RMT), to calculate the complete internal and external elastic lamina muscular artery accounted for a percentage of the total number of small blood vessels in the lung, understand the degree of pulmonary vascular muscle. Fresh lung tissue and immediately fixed line uranyl acetate and lead citrate double staining, transmission electron microscopy pulmonary ultrastructural changes. Found that the shunt rats pulmonary artery pressure higher than that of the corresponding control group, pulmonary hypertension, right ventricular hypertrophy significantly increased pulmonary vascular smooth muscle cell proliferation, pulmonary ultrastructural changes showed intimal thickening, endothelial cell volume increase , was the column broke into the lumen, organelle, the expansion of the endoplasmic reticulum and mitochondria with vacuolization, disintegration shedding some of the endothelial cells, stenosis or occlusion, irregular thinning of the internal elastic layer, the part of the regional faults, smooth muscle cells volume increases, an increase in organelles; treated rats above indicators change than reduce the corresponding shunt group (P lt; 0.05). Thus believe that oral Ang Ⅱ receptor antagonist valsartan can significantly reduce pulmonary artery pressure of pulmonary hypertension in rats, reducing the role of pulmonary vascular smooth muscle cell proliferation.}}

Effect of Valsartan on Pulmonary Artery Smooth Muscle Cell Hyperplasia in Rats

Abstract

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