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目的：研究缺氧对肺动脉平滑肌细胞（ＰＡＳＭＣ）增殖、ＤＮＡ合成和细胞周期的作用，并观察亮氨酸脑啡肽（Ｌ－Ｅｎｋ）和阿片受体阻断剂纳洛酮（Ｎａｌ）的影响．方法：离体培养兔ＰＡＳＭＣ，采用四唑盐比色试验（ＭＴＴ），３Ｈ－ＴｄＲ参入技术和流式细胞仪分析细胞周期等方法，观察ＰＡＳＭＣ增殖、ＤＮＡ合成和细胞周期的变化．结果：ＰＡＳＭＣ缺氧培养１２ｈ，２４ｈ后，ＭＴＴ的Ａ值和３Ｈ－ＴｄＲ参入量分别为（１７９±１９．１）％，（１８５±２０．３）％和（１５８±１３．６）％，（１６７±１７．４）％，比常氧对照组（１００％）显著增加（Ｐ＜０．０１）．缺氧培养２４ｈ后，在Ｇ２，Ｍ期的细胞比例显著升高，Ｇ０，Ｇ１期的细胞比例显著减少（Ｐ＜０．０１）．Ｌ－Ｅｎｋ（１×１０－４ｍｏｌ／Ｌ）可明显抑制缺氧促进ＰＡＳＭＣ增殖和ＤＮＡ合成的作用（Ｐ＜０．０１），该抑制作用可被Ｎａｌ阻断．结论：Ｌ－Ｅｎｋ可抑制缺氧时ＰＡＳＭＣ的增殖和ＤＮＡ的合成作用，该抑制效应是通过阿片受体介导的．
OBJECTIVE: To study the effects of hypoxia on the proliferation, DNA synthesis and cell cycle of pulmonary artery smooth muscle cells (PASMCs) and to observe the effects of leucine enkephalin (L-Enk) and opioid receptor blocker naloxone . Methods: Rabbit PASMC were cultured in vitro. The proliferation, DNA synthesis and cell cycle of PASMC were observed by MTT assay, 3H-TdR incorporation assay and flow cytometry. Results: The A value and 3H-TdR incorporation of PASMC were (179 ± 19.1)%, (185 ± 20.3)% and (158 ± 13.6)%, respectively, (167 ± 17.4)%, which was significantly higher than that of normoxic control group (100%) (P <0.01). After hypoxia for 24 hours, the proportion of cells in G2 and M phases increased significantly, while the proportion of cells in G0 and G1 phase decreased significantly (P <0.01). L-Enk (1 × 10-4 mol / L) significantly inhibited the hypoxia-induced PASMC proliferation and DNA synthesis (P <0.01), which could be blocked by Nal. CONCLUSION: L-Enk inhibits the proliferation and DNA synthesis of PASMC during hypoxia, which is mediated by opioid receptors.