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内皮素在低氧性肺动脉高压大鼠肺内的分布及变化研究
引用本文:杨小东,陈文彬.内皮素在低氧性肺动脉高压大鼠肺内的分布及变化研究[J].华西医科大学学报,2000,31(1):30-33.
作者姓名:杨小东  陈文彬
摘    要:为研究低氧性肺动脉高压时大鼠肺内内皮素的分布和变化,以及其与低氧肺动脉高压的关系,用免疫组织化学染色法确定ET-1在肺内的分布,用族免法测定ET-1逍度。结果;ET-1阳性反应部位主要位于内皮细胞,而在内皮与平滑肌连接处浓度更高。缺氧2小时,ET-1浓度无明显变化,缺氧24后,ET-1水平呈升高趋势,并随着缺氧时间的延长而维持在较高水平。

关 键 词:内皮素  肺动脉高压  大鼠  低氧性

The change and distribution of endothelin-1 in lung of hypoxic pulmonary hypertension rat]
X Yang,W Chen,F Li.The change and distribution of endothelin-1 in lung of hypoxic pulmonary hypertension rat][J].Journal of West China University of Medical Sciences,2000,31(1):30-33.
Authors:X Yang  W Chen  F Li
Institution:Department of Internal Medicine, First Affiliated Hospital, WCUMS, Chengdu 610041.
Abstract:This study was aimed to determine the distribution and change of ET-1 in the lung of rat with chronic hypoxic pulmonary hypertension. Immunohistochemical analysis (Avidin-Biotion Complex) was used to localize the ET-1 immunoreactivity in the rat lung. The ET-1 concentration in plasma and in lung homogenate was measured by radioimmunoassay. In normal rats, the mean ET-1 concentration in venous plasma was 2.25 +/- 0.68 ng/L, in arterial plasma 1.52 +/- 0.63 ng/L and in lung 1.75 +/- 0.46 ng/L. There was no significant increase of ET-1 level in rats exposed to hypoxia for 2 hours, but there was significant increase of ET-1 after 24 hours hypoxia, and the high levels of ET-1 were maintained in the sustained hypoxia. There was significant correlation between the ET-1 level in arterial plasma(or in lung homogenate) and the maen pulmonary artery pressure. Similaryly, there was significant negative correlation between ET-1 in arterial plasma(or in lung homogenate) and PaO2. Immunohistochemical analysis revealed that the ET-1 immunoreactivity was seen in the endothelium of pulmonary arteries, particularly more positive staining was seen in the band between the endothelium and the smooth muscle cells. Chronic hypoxia elevated the mean pulmonary arterial pressure, caused vessel remodelling and the right ventricular hypertrophy. These changes were accompained by an increase of ET-1 in plasma and lung homogenate. The expression and production of ET-1 were localized to endothelium and airway epithelium in the lungs.
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