2002Zhongguo yaolixue tongbaoRequires access

The regulating effect of L-arginine on pulmonary vascular structural remodeling induced by high pulmonary blood flow

Qi Jian

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Abstract

AIM To explore the therapeutic effect of L arginine on pulmonary vascular structural remodeling and pulmonary hypertension induced by high pulmonary blood flow and its mechanism. METHODS Twenty male SD rats were randomly divided into shunting group( n =7), shunting with L arginine group( n =7) and control group( n =6). L arginine was given into stomachs in the rats of shunting with L arginine group (1 g·kg -1 ·d -1 ). Abdominal aorta and inferior vena cava shunting was produced in rats of shunting group and shunting with L arginine group. After 11 week shunting, pulmonary artery mean pressure (mPAP) of each rat was evaluated by using a right cardiac catheterization procedure. The ratio of right ventricular mass to left ventricular plus septal mass (RV/LV+S) was detected. Pulmonary vascular micro and ultra structures were examined. Meanwhile, the expression of human urotensin II (hUⅡ) by pulmonary arteries was detected by immunohistochemistry. RESULTS mPAP and RV/LV+S were significantly increased in shunting rats as compared with those of normal controls ( P 0 01, respectively). Micro structure and ultrastructure of pulmonary arteries changed obviously in shunt rats. Meanwhile, hUⅡ expression by pulmonary artery endothelial cells and smooth muscle cells was significantly augmented in rats of shunting group. However, mPAP and RV/LV+S were significantly decreased in rats of shunting with L arginine group as compared with shunt rats ( P 0 05, respectively). L arginine ameliorated pulmonary vascular structural remodeling in shunting rats in association with an inhibited hUⅡ expression. CONCLU SION L arginine plays an important role in the regulation of development of high pulmonary blood flow induced pulmonary vascular structural remodeling and pulmonary hypertension through inhibiting hUII expression in pulmonary artery endothelial cells and smooth muscle cells.

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AIM To explore the therapeutic effect of L arginine on pulmonary vascular structural remodeling and pulmonary hypertension induced by high pulmonary blood flow and its mechanism. METHODS Twenty male SD rats were randomly divided into shunting group( n =7), shunting with L arginine group( n =7) and control group( n =6). L arginine was given into stomachs in the rats of shunting with L arginine group (1 g·kg -1 ·d -1 ). Abdominal aorta and inferior vena cava shunting was produced in rats of shunting group and shunting with L arginine group. After 11 week shunting, pulmonary artery mean pressure (mPAP) of each rat was evaluated by using a right cardiac catheterization procedure. The ratio of right ventricular mass to left ventricular plus septal mass (RV/LV+S) was detected. Pulmonary vascular micro and ultra structures were examined. Meanwhile, the expression of human urotensin II (hUⅡ) by pulmonary arteries was detected by immunohistochemistry. RESULTS mPAP and RV/LV+S were significantly increased in shunting rats as compared with those of normal controls ( P 0 01, respectively). Micro structure and ultrastructure of pulmonary arteries changed obviously in shunt rats. Meanwhile, hUⅡ expression by pulmonary artery endothelial cells and smooth muscle cells was significantly augmented in rats of shunting group. However, mPAP and RV/LV+S were significantly decreased in rats of shunting with L arginine group as compared with shunt rats ( P 0 05, respectively). L arginine ameliorated pulmonary vascular structural remodeling in shunting rats in association with an inhibited hUⅡ expression. CONCLU SION L arginine plays an important role in the regulation of development of high pulmonary blood flow induced pulmonary vascular structural remodeling and pulmonary hypertension through inhibiting hUII expression in pulmonary artery endothelial cells and smooth muscle cells.

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Available abstract

AIM To explore the therapeutic effect of L arginine on pulmonary vascular structural remodeling and pulmonary hypertension induced by high pulmonary blood flow and its mechanism. METHODS Twenty male SD rats were randomly divided into shunting group( n =7), shunting with L arginine group( n =7) and control group( n =6). L arginine was given into stomachs in the rats of shunting with L arginine group (1 g·kg -1 ·d -1 ). Abdominal aorta and inferior vena cava shunting was produced in rats of shunting group and shunting with L arginine group. After 11 week shunting, pulmonary artery mean pressure (mPAP) of each rat was evaluated by using a right cardiac catheterization procedure. The ratio of right ventricular mass to left ventricular plus septal mass (RV/LV+S) was detected. Pulmonary vascular micro and ultra structures were examined. Meanwhile, the expression of human urotensin II (hUⅡ) by pulmonary arteries was detected by immunohistochemistry. RESULTS mPAP and RV/LV+S were significantly increased in shunting rats as compared with those of normal controls ( P 0 01, respectively). Micro structure and ultrastructure of pulmonary arteries changed obviously in shunt rats. Meanwhile, hUⅡ expression by pulmonary artery endothelial cells and smooth muscle cells was significantly augmented in rats of shunting group. However, mPAP and RV/LV+S were significantly decreased in rats of shunting with L arginine group as compared with shunt rats ( P 0 05, respectively). L arginine ameliorated pulmonary vascular structural remodeling in shunting rats in association with an inhibited hUⅡ expression. CONCLU SION L arginine plays an important role in the regulation of development of high pulmonary blood flow induced pulmonary vascular structural remodeling and pulmonary hypertension through inhibiting hUII expression in pulmonary artery endothelial cells and smooth muscle cells.

Key concepts: Shunting, Pulmonary artery, Medicine, Internal medicine, Arginine, Cardiology, Inferior vena cava, Pulmonary hypertension

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