妊娠高血压综合征合并胎儿生长受限胎盘组织血管细胞粘附分子1的表达

目的：探讨血管细胞粘附分子1（vascular cell adhesion molecule-1,VCAM-1)在妊娠高血压综合征（简称妊高征）合并胎儿生长受限（fetal growth restriction,FGR)发病过程中的作用。方法：采用免疫组化法测定30例妊高征合并FGR患者、28例非妊高征合并FGR及30例正常妊娠者胎盘组织中血管内皮及滋养细胞的VCAM－1表达。结果：妊高征合并FGR组胎盘底蜕膜内血管内皮VCAM－1的表达阳性率（80％）及表达强度（＋＋＋）14例，与正常妊娠组25％（＋＋＋）0例及非妊高征合并FGR组155％（＋＋＋）0例相比明显增高（P＜0．005），而前两者间无显著差异，随妊高征病情加重，其表达强度逐渐增强；胎盘绒毛毛细血管VCAM－1阳性表达强度妊高征合并FGR组（73．3％）和非妊高征FGR组（67．8％）明显增强，与正常组（10％）相比差异有显性（P＜0．005）；所有GFR患者胎盘滋养细胞VCAM－1表达强度明显降低（妊高征FGR为0％，非妊高征FGR组3．6％，正常组40％），并且在妊高征组随妊高征病情加重其表达强度急剧减低。结论：胎盘血管内皮及绒毛滋养细胞异常表达的VCAM－1参与了妊高征引起FGR的病理生理过程，可以作为判定妊高征对胎盘损伤程度的一个指标。

Expression of Vascular Cell Adhesion Molecule-1(VCAM-1) in Placenta of Pregnancy Induced Hypertension Complicated by Fetal Growth Restriction

Objective To investigate the role of vascular cell adhesion molecule 1 (VCAM 1) in pathogenesis of pregnancy induced hypertension (PIH) complicated by fetal growth restriction (FGR). Methods The placenta samples were collected from 30 pregnant women with PIH complicated by FGR, 28 FGR patients without PIH and 30 normal pregnant women. Immunohistochemical analysis was used to demonstrate the positive expression of VCAM 1 in placenta vascular endothelium and syncytiotrophoblast of these samples. Results In placentas of PIH complicated by FGR (80%),expression of VCAM 1 in the decidual vascular endothelium was significantly higher than those without PIH (25%) and normal placentas (15%)( P<0.005 ). There are no significant differences between former two groups. The positive expression increased as the PIH advanced in PIH complicated by FGR group and it was significantly higher in villous capillary vessel of PIH complicated by FGR group (73.3%) and GFR without PIH group (67.8%) ( P< 0.005 ), and there are no significant differences between them. There was significantly low expression of VCAM 1 in syncytiotrophoblast in all FGR placentas and the positive expression extremely decrease with PIH advanced in PIH complicated by FGR group. Conclusions Abnormal expression of VCAM 1 in placenta vascular endothelium and syncytiotrophoblast might participate in pathogenesis of PIH complicated by FGR and as an index for injury of placenta by PIH.