慢性低氧对大鼠肺外肺动脉胶原基因表达的影响

EHect of Chronic Hypoxia on Gene Expression of Collagen in Rats Extrapulmonary Arteries

复制常压低氧性肺动脉高压大鼠模型。测定肺动脉压、右心室收缩压及右心室重，用分子杂交法测定肺动脉、胸主动脉及右心室前胶原Ⅰ、Ⅲ型ｍＲＮＡ表达水平的变化和７６４－３处理对其影响。结果发现，低氧７天时肺动脉压、右心室收缩压及右心室重量显著增加。斑点印迹杂交分析显示肺外肺动脉中前胶原Ⅰ型ｍＲＮＡ表达水平显著增加。７６４－３处理可显著缓解上述变化。肺动脉中前胶原Ⅲ型ｍＲＮＡ表达水平各组间无明显差异。胸主动脉及右心室壁组织中前胶原Ⅰ、Ⅲ型ｍＲＮＡ表达水平各组间均无明显差异。提示低氧性肺动脉高压时，肺动脉中主要是以Ⅰ型胶原合成增多。

ypoxic pulmonary hypertension rats moddle was reproduced by normobaric hypoxia. Pulmonary arterialpressure(PAP) ,right ventricular systolic pressure(RVSP)and the ratio of weight of right ventricle to left ventri-cle plus septum(RV/(LV+S))were measured. Changes of proα_1(Ⅰ), proα_1(Ⅲ) collagen mRNA and β-actinmRNA in extrapulmonary arteries (EPA),thoracic aorta and right ventricle were measured by molecular hy-bridization and observed the effect of 764-3 on it.Results showed that PAP , RVSP and RV/(LV + S) were significantly increased in hypoxic group. 764-3obviously attenuated this increase. Dot blot analysis showed that hypoxia increased the level of proα_1(Ⅰ) collagenmRNA in EPA. 764-3 prevented this increase too. There were no differences in the levels of pro α _1(Ⅲ)collagenmRNA,β-actin mRNA of EPA between any two groups。 The levels of pro α _1(Ⅰ), proα(Ⅲ)collagen mRNAand β-actin mRNA in thoracic aorta and right ventricle showed no differences between any two groups.The results suggested that increased type Ⅰ collagen gene expression contribtites to collagen accumulation inhypoxic hypertensive pulmonary arteries. 764-3 inhibits typeⅠ collagen gene expression. Which may play an rolein attenuated the hypoxic hypertension.