Comparison of Vascular Responses to Vasoconstrictors in Human Placenta in Preeclampsia between Preterm and Later Term

Comparison of Vascular Responses to Vasoconstrictors in Human Placenta in Preeclampsia between Preterm and Later Term
复制标题

早产儿和晚期子痫前期人胎盘血管收缩剂的血管反应比较

DOI:
10.2174/1389201021666191217114111
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发表时间:
2020-01-01
影响因子:
2.8
通讯作者:
Xu, Zhice
Xu, Zhice
中科院分区:
医学4区
文献类型:
--
作者:
Feng, Xueqin;Zhang, Yumeng;Xu, Zhice

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背景:胎盘血管在母胎循环中起着重要作用。尽管先兆子痫的病理机制尚不清楚,但已知胎盘血管功能障碍可能导致妊娠期高血压。然而,早产时胎盘微血管功能或功能障碍的研究尚未见报道。方法:从早产和足月正常妊娠和先兆子痫妊娠获得胎盘。胎盘微血管被用来测定血管张力和对各种血管收缩药的反应以及细胞内钙存储能力。结果:与对照组相比,晚期子痫前期组胎盘血管对血管紧张素II和咖啡因的收缩反应显著降低,而对氯化钾、内皮素-1和缓激肽的反应无明显改变。在早产和晚产胎盘微血管张力的比较中,咖啡因和5-羟色胺诱导的早产血管收缩明显弱于晚产。相反,早产儿先兆子痫患者对血管紧张素II的血管反应增强,而KCl-、内皮素-1和缓激肽介导的胎盘血管反应与晚期子痫前期相似。结论:新数据显示微血管对血管紧张素II和5-羟色胺的反应。胎盘组织中ET-1和缓激肽的活性在早产时显著降低,细胞内钙离子储存能力也受到损害,为胎盘血管功能障碍在妊娠高血压疾病中的可能作用提供了重要信息。
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 bradylcinin-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 Ca(2+ )store capacity was damaged too, providing important information on possible contributions of placental vascular dysfunction to pregnant hypertension.