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目的和方法：应用免疫组织化学、原位末端标记技术及Ｎｏｒｔｈｅｒｎ杂交等方法检测慢性缺氧大鼠肺内特别是肺血管壁细胞增殖、凋亡及相关基因ｃｍｙｃ、ｐ５３表达。结果：正常及慢性缺氧大鼠肺内检出一定比率的增殖、凋亡阳性细胞，两类细胞在肺内呈不均匀散在分布。在缺氧大鼠肺内，增殖阳性细胞绝大部分是肺小血管壁细胞，凋亡性染色细胞在肺小血管壁上较对照组少见。缺氧１、２周组大鼠肺内细胞增殖指数显著增高而凋亡指数显著减少，细胞增殖凋亡比值分别约为对照组３与３５倍。ｃｍｙｃ及ｐ５３是细胞增殖、凋亡密切相关的两种癌（抑癌）基因，前者在缺氧大鼠肺内表达显著增加，而后者（野生型）表达显著减少。结论：可能由于ｃｍｙｃ及ｐ５３基因异常表达所致的细胞增殖、凋亡失衡参与了慢性缺氧性肺血管结构改建的调节。
PURPOSE AND METHODS: The proliferation, apoptosis and the expression of c-myc, p53 in the lung, especially the pulmonary vascular wall, in chronic hypoxic rats were detected by immunohistochemistry, in situ end labeling and Northern blotting. Results: A certain percentage of proliferating and apoptotic cells were detected in the lungs of normal and chronic hypoxia rats. The two types of cells were unevenly distributed in the lungs. In hypoxic rat lung, the majority of proliferating positive cells were small pulmonary artery wall cells, and apoptotic stained cells were rare in the small pulmonary vascular wall than the control group. Compared with the control group, the proliferation index and apoptotic index of hypoxia group were significantly increased (P <0.05). c-myc and p53 are two kinds of cancer (tumor suppressor) genes closely related to cell proliferation and apoptosis. The former is significantly increased in the lungs of hypoxia rats and the latter is significantly decreased. Conclusion: The imbalance of apoptosis may be involved in the regulation of chronic hypoxic pulmonary vascular remodeling possibly due to the proliferation of c-myc and p53 gene.