妊娠期高血压疾病患者血管活性物质检测及其临床意义

Clinical significance of changes of vasodilator and vasoconstrictor factors in patients with pregnancy induced hypertension

目的检测正常妊娠妇女和妊娠期高血压疾病患者外周血中舒血管活性物质与缩血管活性物质的含量并探讨它们的变化在妊娠期高血压疾病发病机制中的作用。方法实验分妊娠期高血压疾病组(87例)、正常妊娠妇女组(81例)和非孕妇女组(27例)。外周血中CGRP、NPY及ET的含量运用放射免疫法、NO的含量运用镉柱比色法分别进行检测。结果妊娠期高血压疾病组的血浆舒张因子NO的含量与正常妊娠组晚孕妇女相比差异无显著性(P>0.05);妊娠期高血压疾病组患者血浆CGRP的含量明显低于正常妊娠组晚孕妇女(P<0.05),并随病情的加重而降低,与其平均动脉压呈显著负相关(r=-0.57,P<0.05)。妊娠期高血压疾病组的NPY和ET的含量均显著高于正常妊娠组(P<0.01),并且均随病情的严重程度的增加而增加(P<0.05)。妊娠期高血压疾病组血浆收缩/舒张因子(NPY+ET)/(VEGF+CGRP+NO)的比值明显大于妊娠组和正常组(P<0.05)。结论妊娠后血管收缩与舒张因子系统平衡失调在妊娠期高血压疾病的发病机制中发挥重要作用。

[Objective] To determine the contents of blood vadedilator nitric oxide （NO）, calcitonin gene-related peptide （CGRP） and vasoconstrictor endothelin （ET）, neuropeptide Y （NPY） in patients with pregnancy induced hypertension （PIH） as well as to explore the pathognensis of pregnancy induced hypertension. [Methods] The plasma CGRP, ET and NPY contents in 27 nonpregnant women （normal group）, 81 healhy pregnant women （control group） and 87 patients with PIH （PIH group） were determined by radioimmunoassay, and the plasma NO content was determined by cadmium-column reduction spectro-photometry. [Results] Compared with late pregnancy women of control group, the plasma NO content of PIH were not significantly increased （P 〉0.05）, and the plasma CGRP content of PIH group was significantly decreased （P 〈0.05）, and there was a trend that plasma CGRP content decreased with the severity of PIH and a negative relationship with the mean arterial blood pressure （mABP, γ= -0.57, P 〈0.05）. The plasma vasoconstrictor NPY and ET contents of PIH group were significantly higher than those of control group （P 〈0.01）, and increased with the severity of PIH. The ratio of plasma vasoconstrictor（NPY＋ET）/vasedilator（CGRP＋NO） in PIH group was significantly higher that of control and normal group（P 〈0.05）. [Conclusion] Imbalance between vasoconstrictor and vasodilator or increased ratio of vasoconstrictor/vasodilator may play an important role in the pathogenesis of PIH.