CO作用后大鼠肺血管细胞增殖和凋亡状况的研究

目的：通过研究CO和低氧作用后大鼠肺血管细胞增殖和凋亡状况，探讨低氧肺动脉高压的发病机制及防治措施。方法：应用免疫组织化学，原位末端标记及Western杂交等方法检测常压低氧大鼠肺血管壁细胞增殖，凋亡及c-myc基因的表达状况。结果：正常组，低氧和锡原卟啉组，低浓度CO和血晶素组大鼠肺动脉均存在增殖和凋亡的阳性细胞，两类细胞在肺内呈不均匀散在分布，低氧和锡原卟啉组大鼠肺血管增殖细胞数显著升高而凋亡细胞数显著减少，细胞增殖凋亡比值分别为对照组的5倍或4倍，而低浓度CO和血晶素组肺血管增殖细胞和凋亡细胞系数均显著增加，细胞增殖凋亡比值均为1．2，c-myc在低氧和锡原卟啉组大鼠肺内表达显著增加，在低浓度CO和血晶素组大鼠肺内表达减少。结论：增殖和凋亡现象共存在于正常和处理大鼠的肺血管细胞中，也许c-myc等基因的异常表达导致了细胞增殖和凋亡的失衡，进而调节了慢性低氧肺血管结构的改建。

Effect of carbon monoxide on cell proliferation and apoptosis inhypoxic pulmonary vessels in rats

Objective To study the effect of CO on cell proliferation and apoptosis in pulmonary vessels of rats after hypoxia for the pathogenesis and treating measures of hypoxic pulmonary hypertension. Methods A total of 60 Wistar rats were randomly and equally devided into 5 groups, i.e. control, hypoxia, hemin, SnPP, and CO groups. Immunohistochemical method, in situ terminal transferase labeling, and Western blot were used to investigate the condition of proliferation and apoptosis, and the expression of c myc in hypoxic pulmonary vascular tissues. Results The proliferative and apoptotic pulmonary arterial smooth muscle cells were seen sparsely in rat lungs of all groups. The proliferative cells were significantly increased but the apoptotic cells decreased in lungs of hypoxia and SnPP groups, by 5 and 4 folds respectively compared with those of control. But in the CO and hemin groups, the proliferation cells and the apoptotic cells were increased dramatically, both by folds of 1.2 in comparison with control. The expression of c myc in lungs of hypoxia and SnPP groups was elevated obviously, but decreased significantly in CO and hemin groups. Conclusion The proliferation and apoptosis are co existent in pulmonary vessels of normal and aberrant rats. It might be the abnormal expression of c myc which leads to the unbalance of proliferation and apoptosis, and then contributes to pulmonary vascular structural remodeling.