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目的：观察内源性阿片肽Ｌ－Ｅｎｋ、吗啡对兔肺动脉平滑肌细胞增殖作用的影响并分析其作用机制．方法：离体培养新西兰兔肺动脉平滑肌细胞（ＰＡＳＭＣ），采用四唑盐比色法（ＭＴＴ）和３Ｈ－ＴｄＲ参入实验观察ＰＡＳＭＣ增殖和ＤＮＡ合成量的变化．结果：Ｌ－Ｅｎｋ对ＰＡＳＭＣ增殖及ＤＮＡ合成有抑制作用且呈剂量依赖效应．Ｌ－Ｅｎｋ（１×１０－３～１×１０－４ｍｏｌ／Ｌ）对ＰＡＳＭＣ的增殖和ＤＮＡ的合成有显著的抑制作用，该作用可被阿片受体阻断剂纳络酮阻断．吗啡对ＰＡＳＭＣ的增殖和ＤＮＡ的合成无显著影响．结论：内源性阿片肽可能主要是通过δ亚型阿片受体对ＰＡＳＭＣ的生长、增殖起抑制作用的，而与μ亚型阿片受体无明显关系．阿片肽类递质抑制ＰＡＳＭＣ增殖作用的可能机制是通过抑制原癌基因ｃ－ｍｙｃ、ｃ－ｆｏｓ的表达从而抑制细胞从Ｇ１进入Ｓ期．
OBJECTIVE: To observe the effect of endogenous opioid peptide L-Enk and morphine on the proliferation of pulmonary artery smooth muscle cells in rabbits and to analyze its mechanism. Methods: Pulmonary artery smooth muscle cells (PASMCs) of New Zealand rabbits were cultured in vitro. The proliferation and DNA synthesis of PASMCs were observed by MTT assay and 3H-TdR incorporation assay. Results: L-Enk inhibited the proliferation and DNA synthesis of PASMC in a dose-dependent manner. L-Enk (1 × 10-3 ~ 1 × 10-4mol / L) significantly inhibited the proliferation and DNA synthesis of PASMC, which could be blocked by opioid receptor blocker naloxone. Morphine had no significant effect on PASMC proliferation and DNA synthesis. CONCLUSION: Endogenous opioid peptides may inhibit the growth and proliferation of PASMC primarily through δ-subtype opioid receptors, but not with μ-subtype opioid receptors. Opioid peptides neurotransmitters inhibit the proliferation of PASMC may be a mechanism by inhibiting the protooncogene c-myc, c-fos expression thereby inhibiting cells from the G1 into the S phase.