Xiao F, Che D Y, Zhang W R
Department of Pathology, Tongji Medical University, Wuhan.
J Tongji Med Univ. 1993;13(1):10-3. doi: 10.1007/BF02886585.
The direct effect of hypoxia and the effect of hypoxic endothelial cells conditioned medium on cultured pulmonary arterial smooth muscle cells in vitro were studied with phase contrast in microscopy, 3H-thymidine labelled technique and flow cytometric measurements. The results showed that direct hypoxia inhibited proliferation of pulmonary arterial smooth muscle cells, retained pulmonary arterial smooth muscle cells in the Go/G1 phase and decreased 3H-thymidine incorporation into pulmonary arterial smooth muscle cells and that hypoxic endothelial cells conditioned medium stimulated proliferation of pulmonary arterial smooth muscle cells, promoted pulmonary arterial smooth muscle cells from G0/G1 phase to S phase and increased 3H-thymidine incorporation into pulmonary arterial smooth muscle cells. It was reasonable to believe that hypoxia might enable pulmonary arterial endothelial cells to secrete some growth factors which could stimulate proliferation of pulmonary arterial smooth muscle cells, thereby playing an important role in structural remodeling of the pulmonary arteries and in the development of hypoxic pulmonary hypertension.
采用相差显微镜、3H-胸腺嘧啶核苷标记技术及流式细胞仪检测，研究了低氧的直接作用以及低氧内皮细胞条件培养液对体外培养的肺动脉平滑肌细胞的影响。结果显示，直接低氧抑制肺动脉平滑肌细胞增殖，使肺动脉平滑肌细胞停滞于G0/G1期，减少3H-胸腺嘧啶核苷掺入肺动脉平滑肌细胞；而低氧内皮细胞条件培养液刺激肺动脉平滑肌细胞增殖，促使肺动脉平滑肌细胞从G0/G1期进入S期，增加3H-胸腺嘧啶核苷掺入肺动脉平滑肌细胞。有理由认为，低氧可能使肺动脉内皮细胞分泌某些生长因子，刺激肺动脉平滑肌细胞增殖，从而在肺动脉结构重塑及低氧性肺动脉高压的发生发展中起重要作用。
