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目的探讨血小板活化、黏附、聚集功能变化在妊娠期高血压疾病(hypertensivedisor-dercomplicatingpregnancy,HDCP)的发生发展中的作用。方法设立正常非孕组(40例)、正常妊娠组(40例)和HDCP组(共60例,妊娠期高血压、轻度子前期和重度子前期分别为25、20和15例),以流式细胞数测定血小板总数,以放射免疫法测定血小板颗粒膜旦白(GMP-140)、ELISA法测定血栓烷B2(TXB2)、β-血小板球旦白(β-TG)、测量血小板黏附率(PAdT)和血小板聚集率(PagT)。结果(1)正常非孕组、正常妊娠组、HDCP组血小板数分别为(206±48)×109/L、(204±52)×109/L和(168±51)×109/L,HDCP组显著低于其它两组(P<0.05);(2)正常妊娠组与正常非孕组GMP-140分别为(12.2±3.8)μg/L、(7.9±2.8)μg/L,TXB2分别为(80.0±39.6)ng/L、(73.6±40.8)ng/L,β-TG分别为(18.5±9.8)μg/L、(16.3±9.5)μg/L,正常妊娠组各指标均较正常非孕组明显升高(P<0.05);而HDCP组GMP-140、TXB2和β-TG分别为(25.1±3.8)μg/L、(107.6±32.8)ng/L和(23.9±9.2)μg/L,较正常非孕组和正常妊娠组明显升高(P<0.01);(3)正常非孕组、正常妊娠组、HDCP组血小板黏附率(PAdT)分别为(18±9)%、(20±8)%和(30±10)%,血小板聚集率(PagT)分别为(28±10)%、(29±10)%和(40±12)%,HDCP组高于正常非孕组和正常妊娠组(P<0.01),并随病情加重而呈增高趋势。结论血小板的活化、黏附、聚集功能的改变可能参与了HDCP的发生、发展过程。
Objective To investigate the role of platelet activation, adhesion and aggregation in the development and progression of hypertensive disease-of-hypertension (HDCP). Methods Normal non-pregnant group (40 cases), normal pregnancy group (40 cases) and HDCP group (60 cases, pre-pregnancy gestational hypertension, mild premature ejaculation and severe premature ejaculation were 25, 20 and 15 cases) , The total number of platelets was determined by flow cytometry, GMP-140 was measured by radioimmunoassay, TXB2 and β-TG were measured by ELISA, Adhesion rate (PAdT) and platelet aggregation rate (PagT). Results The number of platelets in normal non-pregnant group, normal pregnancy group and HDCP group were (206 ± 48) × 109 / L, (204 ± 52) × 109 / L and (168 ± 51) × 109 / L, (12.2 ± 3.8) μg / L and (7.9 ± 2.8) μg / L, respectively. The levels of TXB2 in normal pregnancy group and normal non-pregnant group were (80.0 ± 39.6) ng / L and (73.6 ± 40.8) ng / L, respectively. The levels of β-TG were (18.5 ± 9.8) μg / L and The levels of GMP-140, TXB2 and β-TG in HDCP group were (25.1 ± 3.8) μg / L, (107.6 ± 32.8) ng / L and (23.9 ± 9.2) μg / (P <0.01); (3) The platelet adhesion rate (PAdT) in normal non-pregnant group, normal pregnancy group and HDCP group were (18 ± 9)%, (28 ± 10)%, (29 ± 10)% and (40 ± 12)%, respectively, which were significantly higher in HDCP group than those in normal non-pregnant group (20 ± 8% vs 30 ± 10% And normal pregnancy group (P <0.01), and increased with the increase of the disease. Conclusion The changes of platelet activation, adhesion and aggregation may be involved in the occurrence and development of HDCP.