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目的：探讨妊高征患者内皮细胞功能紊乱时ET/CGRP的变化及孕激素所起的作用。方法：体外原代培养8例妊高征患者的脐静脉内皮细胞，待细胞融合为单层后，分为四组各分别加入正常孕妇血清、妊高征患者血清、妊高征患者血清及孕激素、等量的1640培养液，均置于37℃、5%的CO2培养箱中培养24h，收集培养液，应用放射免疫法测定其中CGRP及ET的含量变化。结果：第二组与第一组比较，CGRP明显下降，ET明显升高，ET/CGRP见明显差异；第三组与第一组比较，CGRP无变化，ET明显升高，ET统计学意义上的差异；第二组与第三组比较，CGRP明显下降，ET无变化，ET/CGRP有统计学意义上的差异。结论：血管内皮损伤可能是妊高征发病中的重要环节，细胞毒性因子引致的血管内皮细胞功能紊乱引发或加剧了ET/CGRP的平衡失调，致血管收缩效应占优势，在妊高征的发病中起着不容忽视的作用；孕激素与了CGRP的生物效应过程，在妊高征的发展过程中与CGRP可能共同起到延缓作用。
Objective: To investigate the changes of ET / CGRP and the role of progesterone in endothelial dysfunction in patients with pregnancy induced hypertension (PIH). Methods: Umbilical vein endothelial cells from 8 patients with PIH were cultured in vitro. When the cells were confluent into monolayer, they were divided into four groups, which were respectively added into serum of normal pregnant women, serum of patients with PIH, serum of patients with PIH and pregnancy Hormone, equal amount of 1640 culture medium, were placed in 37 ℃, 5% CO2 incubator cultured 24h, the culture medium was collected, the content of CGRP and ET were measured by radioimmunoassay. Results: Compared with the first group, the CGRP decreased significantly in the second group and the ET increased significantly, while the ET / CGRP showed obvious difference. In the third group, compared with the first group, CGRP remained unchanged and ET significantly increased The difference between the second group and the third group, CGRP decreased, ET did not change, ET / CGRP differences were statistically significant. Conclusion: The vascular endothelial injury may be an important link in the pathogenesis of PIH. The dysfunction of vascular endothelial cells induced by cytotoxic factors may cause or aggravate the imbalance of ET / CGRP and lead to the vasoconstrictor effect. In the pathogenesis of PIH, Plays a role that can not be ignored; progesterone and the biological effects of CGRP process, in the development of pregnancy-induced hypertension and CGRP may play a role in delaying.