中文摘要：

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。

英文摘要：

Objective： To explore microvessel density （MVD） of villus and decidua in the first trimester, the last trimester and in pregnancies complicated by preeclampsia and the concentration of VEGF in corresponding groups, and then understand the mechanism of angiogenesis in normal pregnancy and preeclampsia. Methods： In placentas and deciduas tissues from 16 cases of normal early pregnancy, 27 cases of term pregnancy and 45 cases of pregnancy complicated with preeclampsia （21 cases of mild and 24 cases of severe preeclampsia）, immunohistochemistry was used to detect the protein expression of MVD. ELISA were used to detect the concentrations of VEGF in corresponding serum. Results ： The MVD at higher power magnification in placentas of normal early pregnancy, 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; and the MVD at higher power magnifica- tion in deciduas of normal early pregnancy, term pregnancy, mild preeclampsia and severe preeclampsia were 8.38 ±3.40, 98. 67±7.41, 88.96 ± 8.79 and 66. 05±10. 17. The concentrations of VEGF in the corresponding serum were （90. 62 ±15.68 ） pg/ml, （ 118. 94± 20. 06） pg/ml, （ 107.38 ± 17. 84） pg/ml, （42. 73 ±8. 50） pg/ml. The MVDs in early pregnancies were lower, especially in deciduas; the MVDs in placentas and deciduas were no significant differences between term pregnancy and mild preeclampsia, but MVDs observed in severe preeclampsia decreased dramatically （P 〈 0. 05 ） . The same result could be seen in the corresponding serum （P 〈0. 05 ） . Conclusion： Angiogenesis participates the course of placentation, and may play an important part in the pathogenesis of pre - eclampsia.