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目的:探讨肾上腺髓质素(AM)在低氧性肺动脉高压(HPH)形成过程中的作用。方法:将大鼠随机分为对照组,低氧1,3,5,7,10,14,21d组。采用常压间断低氧法制作HPH模型;放免法测定血浆和肺匀浆AM及内皮素1(ET-1)浓度;采用RNA印迹法检测肺组织AM受体mRNA表达情况。结果:(1)低氧第3天,血浆AM浓度即显著升高(P<0.05),至第14天达高峰。(2)ET-1/AM比值从低氧第1天即开始升高,7～10d达到高峰(P<0.01)。肺匀浆AM浓度到低氧14d方出现显著升高。(3)AM受体mRNA表达相对值在低氧第3天明显降低(P<0.05),到低氧第10天又恢复至正常水平。结论:AM可能作为一种保护性因子参与了HPH的发病过程;AM受体mRNA在低氧早期的下调,可能加剧了HPH的进展。
Objective: To investigate the role of adrenomedullin (AM) in the formation of hypoxic pulmonary hypertension (HPH). Methods: The rats were randomly divided into control group, hypoxia 1,3,5,7,10,14,21 d group. The model of HPH was established by intermittent hypoxia at normal pressure. The concentrations of AM and ET-1 in plasma and lung homogenate were determined by radioimmunoassay. The expression of AM receptor mRNA in lung tissue was detected by Northern blotting. Results: (1) On the third day after hypoxia, plasma AM concentration increased significantly (P <0.05) and peaked on the 14th day. (2) The ET-1 / AM ratio increased from day 1 of hypoxia to peak (P <0.01) at 7-10 days. Lung homogenate AM concentration to hypoxia 14d side significantly increased. (3) The relative value of AM receptor mRNA expression decreased significantly on the 3rd day of hypoxia (P <0.05), and returned to the normal level on the 10th day of hypoxia. Conclusion: AM may participate in the pathogenesis of HPH as a protective factor. The down-regulation of AM receptor mRNA in hypoxia may aggravate the progression of HPH.