【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 ,提示金属蛋白酶可能参与了肺动脉高压及肺血管重建的形成更多还原

【Abstract】 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.更多还原