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用放射免疫测定和免疫组化法观察缺氧对培养的小牛肺动脉内皮细胞（ＰＡＥＣ）和肺动脉平滑肌细胞（ＰＡＳＭ）自分泌心钠素（ＡＮＰ）、血管紧张素Ⅱ（ＡＴⅡ）和内源性洋地黄因子（ＥＤＬＦ）的影响。无氧培养２４ｈ末，ＰＡＥＣ分泌ＡＮＰ减少４３．５％（Ｐ＜０．００１），ＡＴⅡ和ＥＤＬＦ呈明显负相关（ｒ为－０．８８和－０．７８６，Ｐ＜０．０１），细胞内ＡＮＰ阳性颗粒也显著减少（Ｐ＜０．００１）；ＰＡＳＭ分泌ＡＮＰ无显著改变，而细胞内ＡＮＰ明显减少（Ｐ＜０．００１），ＰＡＳＭ分泌ＡＮＰ与ＥＤＬＦ呈正相关（ｒ＝０．７２２，Ｐ＜０．０１），与ＡＴⅡ呈负相关（ｒ＝－０．８６５，Ｐ＜０．０１）。结果表明：缺氧时ＰＡＥＣ和ＰＡＳＭ的ＡＮＰ、ＡＴⅡ和ＥＤＬＦ等自分泌的改变可能参与缺氧性肺血管收缩及结构的改建。
Radioimmunoassay and immunohistochemistry were used to observe the effects of hypoxia on the secretion of atrial natriuretic peptide (ANP), angiotensin Ⅱ (ATⅡ) and endogenous endothelium in cultured pulmonary arterial endothelial cells (PAECs) and pulmonary arterial smooth muscle cells (PASM) Influence of digitalis (EDLF). After anaerobic incubation for 24 h, PAEC secreted ANP decreased by 43.5% (P <0.001), ATⅡ and EDLF showed a significant negative correlation (r = -0.88 and -0.786, P <0.01) (P <0.001). There was no significant change of ANP secretion in PASM, but significant decrease of intracellular ANP (P <0.001). There was a positive correlation between ANP and EDLF secretion of PASM (r = 0.722, P <0.01), but negatively correlated with ATⅡ (r = -0.865, P <0.01). The results showed that the autocrine changes of ANP, ATⅡ and EDLF in hypoxic PAEC and PASM may be involved in the hypoxic pulmonary vasoconstriction and structural remodeling.