Bhavina K, Radhika J, Pandian S Sundara
SRM Medical College Hospital & Research Center, Kattankulathur, Kanchipuram, Tamil Nadu 603203, India.
Biomed Res Int. 2014;2014:982159. doi: 10.1155/2014/982159. Epub 2014 May 14.
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.
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.
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.
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.
妊娠期高血压患者血流减少可能影响血管收缩剂的产生；随后血管处于高度收缩状态。一氧化氮（NO）是一种血管舒张剂；血管内皮生长因子（VEGF）通过调节内皮型一氧化氮合酶（eNOS）的产生影响其合成。我们研究的目的是评估VEGF和eNOS在不同严重程度妊娠期高血压中的表达。
研究纳入4组，每组40人：第1组为对照组，第2组为妊娠期高血压组，第3组为轻度子痫前期组，第4组为重度子痫前期组。采集脐带胎儿端，按照VEGF和eNOS抗体的免疫组化染色方案进行操作。采用半定量评分法测量染色强度。采用曼-惠特尼U检验对各组进行比较。
与正常情况相比，高血压状态下VEGF和eNOS的表达均降低。在高血压组中，重度子痫前期组的染色强度高于妊娠期高血压组和轻度子痫前期组。
妊娠期高血压中VEGF和eNOS的减少可能导致妊娠期高血压患者胎儿灌注不足及随后的缺氧。所形成的缺氧状态可能上调VEGF的合成，从而上调eNOS的合成。重度组中VEGF和eNOS表达增加可能是一种扩张血管并改善胎儿血流的代偿机制。
