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目的：探讨慢性缺氧性肺动脉高压肺血管结构改建（ｐｕｌｍｏｎａｒｙｖａｓｃｕｌａｒｓｔｒｕｃｔｕｒａｌｒｅｍｏｄｅｌｉｎｇ，ＰＶＳＲ）的细胞及分子机制。方法：大鼠慢性缺氧模型复制，免疫组化及Ｎｏｒｔｈｅｒｎ杂交检测大鼠肺内ｃ－ｍｙｃ及ｂｃｌ－２两基因蛋白及ｍＲＮＡ的表达，免疫组化及原位缺口末端标记法检测大鼠肺内增殖相关抗原Ｋｉ－６７及凋亡细胞。结果：正常及慢性缺氧大鼠肺内均检出一定比率的增殖或凋亡细胞，缺氧１、２周大鼠肺内细胞增殖／凋亡比值比对照组分别增高约３、３５倍。与细胞增殖、凋亡密切相关的ｃ－ｍｙｃ、ｂｃｌ－２基因表达在缺氧１周大鼠肺内显著增高，在缺氧２周更显著。结论：细胞增殖、凋亡机制共同参与了慢性缺氧性肺动脉高压时ＰＶＳＲ的调节。
Objective: To investigate the cellular and molecular mechanisms of pulmonary vascular structural remodeling (PVSR) in chronic hypoxic pulmonary hypertension. Methods: The expression of c-myc and bcl-2 mRNA and protein in rat lungs were detected by immunohistochemistry and Northern hybridization. The expressions of c-myc and bcl-2 mRNA and protein were detected by immunohistochemistry and in situ nick end labeling Proliferation-related antigen Ki-67 and apoptotic cells. Results: A certain percentage of proliferating or apoptotic cells were detected in the lungs of normal and chronic hypoxic rats, and the ratio of cell proliferation / Times The expressions of c-myc and bcl-2 genes, which are closely related to cell proliferation and apoptosis, were significantly increased in the lungs of rats exposed to hypoxia for one week and more markedly in hypoxia for two weeks. Conclusion: Cell proliferation and apoptosis are involved in the regulation of PVSR in chronic hypoxic pulmonary hypertension.