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作 者:李继武[1] 龚永生[1] 范小芳[1] 胡良冈[1] 郑绿珍[1] 蒋仲荪[1]
机构地区:[1]温州医学院肺心病研究室,浙江温州325027
出 处:《中国病理生理杂志》2003年第5期657-660,共4页Chinese Journal of Pathophysiology
摘 要:目的 :研究基质金属蛋白酶在低O2 高CO2 性肺动脉高压中的作用。方法 :在慢性低氧高二氧化碳肺动脉高压大鼠模型上 ,采用图像分析、免疫杂交、免疫组化、组织原位杂交技术等方法测定不同缺氧时间 ( 1周、2周、3周 )肺细小动脉基质金属蛋白酶 (MMPs)的含量及肺小血管显微结构。结果 :①慢性低O2 高CO2 大鼠的肺动脉平均压 (mPAP)和右心室 (RV)与左心室加室间隔 (LV +S)重量比 (RV/LV +S)随缺氧时间延长而增高 ,显著高于正常对照组 (P <0 0 1)。②光镜下正常对照组肺细小动脉内弹力板自然弯曲 ,平滑肌层未见明显增厚 ,管壁均匀一致 ,而低O2 高CO2 组内弹力板扭曲 ,中膜平滑肌细胞增生 ,管腔明显狭窄。③免疫杂交、免疫组化、原位杂交法发现肺细小动脉MMP - 2、MMP - 9及其mRNA平均吸光度值 ,低O2 高CO2 高于正常对照组 (P <0 0 1) ,且随着低氧时间的延长而升高。结论 :低O2 高CO2 促使基质金属蛋白酶表达升高 。AIM: To investigate the expression of matrix metalloproteinases(MMPs) in pulmonary arterioles of rats with chronic hypoxia and hypercapnia-induced pulmonary hypertension. METHODS: MMP-2, MMP-9 and MMP-2 mRNA, MMP-9 mRNA were observed in pulmonary arterioles by the techniques of immunohistochemistry and in situ hybridization. RESULTS: ①The mean pulmonary artery pressure (mPAP) and weight ratio of right ventricle to left ventricle and septum (RV/LV+S) of hypoxia-hypercapnia groups were higher than those of normal control group ( P<0.01 ). ②Light microscopy showed that vessel wall and media of pulmonary arterioles were thicker in rats of hypoxia-hypercapnia groups than normal control group. There were vessel smooth muscle cell hypertrophy, vessel cavity straitness in hypoxia-hypercapnia group, but no same performance was found in normal control group. ③The expression of MMP-2, MMP-9 and MMP-2 mRNA, MMP-9 mRNA in pulmonary arterioles were significantly higher in rats of hypoxia-hypercapnia groups than control group ( P<0.01 ). CONCLUSION: Expression of matrix metalloproteinases in pulmonary arterioles is enhanced by hypoxia hypercapnia. This may be involved in pulmonary vascular remodeling in rats with pulmonary hypertension.
关 键 词:肺动脉高压 大鼠 肺血管 基质金属蛋白酶 基因表达 图像分析 免疫杂交 免疫组化
分 类 号:R543.2[医药卫生—心血管疾病]
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