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目的 探讨低氧诱导因子 1(HIF 1α)和内皮素 1(ET 1)基因表达在低氧性肺动脉高压发病过程中的变化和作用。方法 复制低氧性肺动脉高压大鼠模型 ,测定平均肺动脉压 ,弹力纤维染色显示腺泡内肺动脉 ,用放射免疫法测ET含量 ,原位杂交方法进行检测HIF 1αmRNA。结果 HIF 1αmRNA在低氧各组腺泡内肺动脉有表达 ,低氧 14d组 (0 2 5 6 9± 0 0 46 8)和低氧 2 8d组 (0 2 2 5 8±0 0 45 3)染色强于低氧 5d组 (0 145 5± 0 0 2 72 )和正常组 (0 110 9± 0 0 2 2 4) ;ET 1mRNA在低氧各组腺泡内肺动脉有表达 ,低氧 14d组 (0 412 2± 0 0 783)和低氧 2 8d组 (0 36 84± 0 0 72 9)染色强于低氧5d组 (0 2 0 17± 0 0 34 9)和正常组 (0 185 5± 0 0 36 1) ,HIF 1α和ET 1基因表达在H14d组和H2 8d组明显增加 (P <0 0 5 )。肺动脉血中ET 1含量在H14d组 [(15 8 78± 2 5 14)pg/ml]和H2 8d组 [(142 93± 2 3 38)pg/ml]明显高于H5d组 [(79 6 8± 12 5 4)pg/ml]和正常组 [(6 5 37± 10 82 )pg/ml](P <0 0 5 ) ;H14d组 [(34 0± 5 8)mmHg]和H2 8d组 [(2 9 0± 4 7)mmHg]的mPAP也明显高于H5d组[(19 0± 3 5 )mmHg]和正常组 [(17 0± 2 8)mmHg](P <0 .0 5 ) ,并且与肺动脉血中ET 1含量呈正比(rs=0
Objective To investigate the changes and roles of hypoxia inducible factor 1 (HIF 1α) and endothelin 1 (ET 1) gene expression in the pathogenesis of hypoxic pulmonary hypertension. Methods Hypoxic pulmonary hypertension rat models were duplicated, mean pulmonary artery pressure (MAP) was measured, pulmonary artery was observed by elastic fiber staining, ET content was measured by radioimmunoassay, and HIF 1α mRNA was detected by in situ hybridization. Results HIF-1α mRNA was expressed in the pulmonary artery of hypoxic groups of acinar cells. The expression of HIF-1α mRNA in the hypoxic group was significantly higher than that in the hypoxia group (0 2 5 6 9 ± 0 0 46 8) and hypoxia group (0 2 25 58 ± 0 0 45 3) (P <0.05), which was higher than that in hypoxia 5d group (0 145 5 ± 0 0 722) and normal group (0 110 9 ± 0 0 2 2 4) 0 412 2 ± 0 0 783) and hypoxia 2 8d group (0 36 84 ± 0 0 72 9) were stronger than those in hypoxia 5d group (0 2 0 17 ± 0 0 34 9) and normal group (0 185 5 ± The expression of HIF-1alpha and ET-1 was significantly increased in H14d and H2 8d groups (P <0.05). The level of ET 1 in pulmonary arterial blood was significantly higher in H14d group than in H5d group [(15 8 78 ± 2 5 14) pg / ml] and H2 8d group [(142 93 ± 2 38) pg / ml] (34 ± 5 8) mmHg] in the H14d group and in the H2 8d group (P <0.05) (29 0 ± 4 7) mmHg] were also significantly higher than those in the H5d group [(19 0 ± 35) mmHg] and the normal group [(17 0 ± 28) mmHg] (P 0 05) And with pulmonary arterial ET 1 content was proportional (rs = 0