Background: Placental blood vessels play important roles in maternal-fetal circulation. Although pathologic mechanisms of preeclampsia are unclear, it is known that placental vascular dysfunction could contribute to pregnant hypertension. However, placental micro-vessel function or dysfunction at preterm has not been investigated.

Methods: Human placentas from normal and preeclamptic pregnancies at preterm and term were obtained. Placental micro-vessels were used for determining vascular tension and responses to various vasoconstrictors as well as intracellular calcium store capability. It was the first time to show vascular responses in placental arteries to angiotensin II, endothelin-1, and other vascular drugs at preterm.

Results: Compared to the control, placental vascular contractile responses to angiotensin II and caffeine were significantly decreased, while placental vascular responses to KCl, endothelin-1, and bradykinin were not significantly altered in the later term group in preeclampsia. In comparison of placental micro-vessel tension between the preterm and later term, caffeine- and serotonin-induced vascular contractions were significantly weaker in the preterm than that in the later term. On the contrary, vascular response to angiotensin II was increased in the preterm preeclampsia, while KCl-, endothelin-1, and bradykinin-mediated placental vessel responses in the preterm preeclampsia were similar to that in later term preeclampsia.

Conclusion: New data showed that micro-vessel responses to angiotensin II and serotonin, not endothelin- 1 or bradykinin, were significantly reduced in the human placentas at preterm, and intracellular Ca2+ store capacity was damaged too, providing important information on possible contributions of placental vascular dysfunction to pregnant hypertension.

背景：胎盘血管在母胎循环中起重要作用。尽管先兆子痫的病理机制尚不清楚，但众所周知胎盘血管功能障碍可能会导致妊娠高血压。但是，尚未研究早产的胎盘微血管功能或功能障碍。

方法：从早产和足月妊娠的正常和先兆子痫中获得人胎盘。胎盘微血管用于确定血管张力和对各种血管收缩剂的反应以及细胞内钙存储能力。这是早产儿首次显示胎盘动脉中对血管紧张素II，内皮素-1和其他血管药物的血管反应。

结果：与对照组相比，子痫前期后期组的胎盘血管对血管紧张素II和咖啡因的收缩反应显着降低，而胎盘对KCl，内皮素-1和缓激肽的血管反应没有明显改变。比较早产和后期的胎盘微血管张力，咖啡因和5-羟色胺诱导的血管收缩在早产中明显弱于后期。相反，在子痫前期中，对血管紧张素II的血管反应增加，而在子痫前期中，KCl，内皮素-1和缓激肽介导的胎盘血管反应与子痫前期相似。

结论：新数据显示，早孕时人胎盘中血管紧张素II和5-羟色胺的微血管反应，而不是内皮素-1或缓激肽，显着降低，并且细胞内Ca2 +储存能力也受到破坏，这为胎盘可能的贡献提供了重要信息。妊娠高血压的血管功能异常。