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首页> 外文期刊>BioMed research international >VEGF and eNOS Expression in Umbilical Cord from Pregnancy Complicated by Hypertensive Disorder with Different Severity
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VEGF and eNOS Expression in Umbilical Cord from Pregnancy Complicated by Hypertensive Disorder with Different Severity

机译：妊娠合并严重程度不同的高血压病患者脐带中VEGF和eNOS的表达

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Background. Reduced blood flow in hypertensive pregnancy may influence the production vasoconstrictors; subsequently the vessel remains in highly contracted state. NO is a vasodilator; VEGF influences its synthesis by regulating eNOS production. Aim of our study was to evaluate the expression of VEGF and eNOS in different severity of hypertensive pregnancy. Methods. Study was conducted in 4 groups with 40 members: group 1-control, group 2-gestational hypertension, group 3-mild preeclampsia, and group 4-severe preeclampsia. Fetal end of umbilical cord was taken and follows IHC staining protocol for VEGF and eNOS antibody. Staining intensity were measured by semiquantitative scoring method. Mann Whitney U test was used to compare each group. Results. Decreased expression of both VEGF and eNOS was found in hypertensive condition than in normal condition. Among hypertensive group, severe preeclamptic group showed more intensity in staining than gestational hypertension and mild preeclampsia. Conclusion. Reduction of VEGF and eNOS in gestational hypertension may lead to hypoperfusion and subsequent hypoxia of fetus in hypertensive pregnancy. The developed hypoxic state may upregulate the synthesis of VEGF and thereby eNOS. Increased expression of VEGF and eNOS in severe group may be a compensatory mechanism to dilate the blood vessels and to improve blood flow of fetus.
机译：背景。高血压孕妇的血流量减少可能会影响血管收缩剂的产生;随后，船只保持高度收缩状态。 NO是血管扩张剂; VEGF通过调节eNOS的产生影响其合成。我们研究的目的是评估不同程度的高血压妊娠中VEGF和eNOS的表达。方法。研究分为4组，共有40名成员：1组为对照组，2组妊娠高血压，3组轻度先兆子痫和4组重度先兆子痫。取出脐带的胎儿末端，并遵循针对VEGF和eNOS抗体的IHC染色方案。染色强度通过半定量评分法测量。曼惠特尼U检验用于比较各组。结果。在高血压状态下，VEGF和eNOS的表达均低于正常状态。在高血压组中，重度先兆子痫组的染色强度高于妊娠高血压和轻度先兆子痫。结论。妊娠期高血压中VEGF和eNOS的减少可能导致胎儿灌注不足和随后的缺氧。发生的低氧状态可能上调VEGF的合成，从而上调eNOS。严重组中VEGF和eNOS的表达增加可能是血管扩张和胎儿血流改善的补偿机制。

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