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目的:检测早、晚期正常妊娠及子痫前期母胎界面的微血管密度,同时测定相应患者体内VEGF浓度。从而探讨血管新生在妊娠发生及子痫前期发病中的可能机制。方法:采用免疫组织化学染色法检测16例正常早期妊娠绒毛及蜕膜,27例足月妊娠和45例子痫前期(其中轻度子痫前期21例,重度子痫前期24例)胎盘及蜕膜中微血管表达情况。同时利用ELISA方法检测相应患者体内VEGF浓度。结果:在每高倍镜视野下正常早孕绒毛、正常足月妊娠、轻度子痫前期及重度子痫前期胎盘中,微血管密度依次为(9.55±5.61)、(98.07±8.18)、(91.36±3.34)、(68.14±7.62);在相应蜕膜组织中,微血管密度依次为(8.38±3.40)、(98.67±7.41)、(88.96±8.79)、(66.05±10.17)。在上述各组对应病例中VEGF浓度依次为(90.62±15.68)、(118.94±20.06)、(107.38±17.84)、(42.73±8.50)pg/ml。早孕期母胎界面微血管密度较低;与正常足月妊娠相比,轻度子痫前期母胎界面血管密度无明显变化,而重度子痫前期胎盘及蜕膜微血管密度明显降低(P<0.05)。早孕期患者体内VEGF浓度略低,正常足月妊娠VEGF浓度加大,轻度子痫前期较足月妊娠无明显变化,但在重度子痫前期患者VEGF浓度明显下降(P<0.05)。结论:母胎界面血管新生在重度子痫前期发病中起到重要作用,且这一过程受到生长因子的调节。
OBJECTIVE: To detect the microvessel density in the early and late stages of normal pregnancy and maternal-fetal interface of preeclampsia and determine the concentration of VEGF in the corresponding patients. In order to explore the possible mechanism of angiogenesis in the occurrence of pregnancy and preeclampsia. Methods: Immunohistochemical staining was used to detect 16 cases of normal early pregnancy villi and decidua, 27 cases of full-term pregnancy and 45 cases of preeclampsia (including mild preeclampsia in 21 cases, severe preeclampsia in 24 cases) placenta and decidua Microvascular expression. At the same time, ELISA method was used to detect the concentration of VEGF in the corresponding patients. Results: The density of microvessels in normal early pregnancy, normal term pregnancy, mild preeclampsia and severe preeclampsia were (9.55 ± 5.61), (98.07 ± 8.18), (91.36 ± 3.34), ) And (68.14 ± 7.62) respectively. The microvessel density in the corresponding decidua was (8.38 ± 3.40), (98.67 ± 7.41), (88.96 ± 8.79) and (66.05 ± 10.17), respectively. The corresponding concentration of VEGF in each group was (90.62 ± 15.68), (118.94 ± 20.06), (107.38 ± 17.84) and (42.73 ± 8.50) pg / ml, respectively. Compared with normal full-term pregnancy, there was no significant change in the blood vessel density at the maternal-fetal interface in mild preeclampsia, while the density of placental and decidual microvessels in severe preeclampsia was significantly decreased (P <0.05). In early pregnancy, the concentration of VEGF in the patients with mild preeclampsia was slightly lower than that in normal pregnancies. The levels of VEGF in normal preeclampsia did not change significantly compared with those in term pregnancies, but significantly decreased in patients with severe preeclampsia (P <0.05). Conclusion: The maternal-fetal interface angiogenesis plays an important role in the pathogenesis of severe preeclampsia, and this process is regulated by growth factors.