Heli Saarelainen, Henna Kärkkäinen, Pirjo Valtonen, Kari Punnonen, Tomi Laitinen, Nonna Heiskanen, Tiina Lyyra-Laitinen, Esko Vanninen, Seppo Heinonen
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引用次数: 9
摘要
背景。我们的目的是评估正常妊娠与合并高血压或子痫前期妊娠(PE)的妊娠期间和妊娠后的内皮功能和炎症标志物。方法与结果。我们测量了32名正常妊娠妇女和28名妊娠中期和产后至少3个月合并高血压疾病的妇女的内皮依赖性肱动脉血流介导的血管舒张(FMD)和高敏c反应蛋白(hsCRP)、白细胞介素-6 (IL-6)和肿瘤坏死因子-α (TNF-α)。妊娠期高血压患者内皮功能增强明显高于正常妊娠,妊娠期平均FMD%为11.0%比8.8% (P = 0.194),产后平均FMD%为8.0%比7.9% (P = 0.978)。妊娠期高血压组炎症标志物浓度较分娩后明显升高(hsCRP 4.5 vs 0.80 mg/L, P = 0.023; IL-6 2.1 vs 1.2 pg/mL, P = 0.006;TNF-α 1.9 vs 1.5 pg/mL, P = 0.030)。炎症标志物与口蹄疫之间无统计学意义的关联。结论。与正常妊娠相比,妊娠晚期高血压妊娠的肱动脉FMD并未减弱,而hsCRP、IL-6和TNF-α的循环浓度与高血压并发症有关。
Flow-mediated vasodilation is not attenuated in hypertensive pregnancies despite biochemical signs of inflammation.
Background. Our objective was to evaluate endothelial function and markers of inflammation during and after pregnancy in normal pregnancies compared to pregnancies complicated with hypertension or preeclampsia (PE). Methods and Results. We measured endothelium-dependent brachial artery flow-mediated vasodilation (FMD) and high sensitive C-reactive protein (hsCRP), interleukin-6 (IL-6), and tumour necrosis factor-α (TNF-α) in 32 women with normal pregnancy and in 28 women whose pregnancy was complicated with hypertensive disorder in the second half of pregnancy and minimum 3-month postpartum. Enhancement of endothelial function was greater in hypertensive than normal pregnancies, the mean FMD% being 11.0% versus 8.8% during pregnancy (P = 0.194) and 8.0% versus 7.9% postpartum (P = 0.978). Concentrations of markers of inflammation were markedly increased in pregnant hypertensive group compared to those after delivery (hsCRP 4.5 versus 0.80 mg/L, P = 0.023, IL-6 2.1 versus 1.2 pg/mL, P = 0.006; TNF-α 1.9 versus 1.5 pg/mL, P = 0.030). There were no statistically significant associations between the markers of inflammation and FMD. Conclusions. Brachial artery FMD was not attenuated in the third trimester hypertensive pregnancies compared to normal pregnancies, whereas circulating concentrations of hsCRP and IL-6 and TNF-α reacted to hypertensive complications.