摘要
目的:检测妊娠高血压综合征(妊高征)患者血浆内源性一氧化碳(CO)、内皮素-1(ET-1)、血小板聚集性(PAg)的水平。方法:分别采用联二亚硫酸盐法、放射免疫法和血小板聚集仪测定20例健康晚孕妇女与61例妊高征患者(轻度19例,中度20例,重度22例)血浆CO、ET-1、全血PAg水平,并进行相关性分析。结果:中、重度妊高征组CO水平较正常晚孕组下降(P<0.01或0.001),重度组较轻度组下降(P<0.01);妊高征各组血浆ET-1与全血PAg水平均较正常晚孕组升高(P<0.05或0.001),重度组较轻度组升高(P<0.01);血浆CO水平与ET-1、PAg间均呈负相关(P<0.05或0.001)。结论:CO可能通过拮抗ET-1的生成或释放、抑制血小板聚集而在妊高征的病理生理过程中发挥重要的生理作用。
Aim: To study the role of CO in pathophysiological changes of pregnancy induced hypertension (PIH). Methods: Plasma levels of carbon monoxide(CO) , endothlin-1 ( ET-1 ) and platelet aggregation(PAg) in 20 cases of normal late pregnant women and 61 cases of patients with PIH ( 19 cases of mild PIH,20 cases of moderate PIH,and 22 cases of severe PIH) were measured by Chalmers dithionite reduction methods,radioimmunoassay, and platelet aggregation machine, respectively. Results:Compared with normal pregnant women, plasma CO level in PIH groups decreased (P 〈 0.01 or 0.001 ). The plasma ET-1 level and platelet aggregation were higher in PIH groups than those of normal pregnant women (P 〈0.05 or 0. 001 ). The plasma CO level was negatively correlated with ET-1 and platelet aggregation in all groups( P 〈 0.05 or 0.001). Gonclusion: CO may be one of the antagonists of ET-1 and platelet aggregation in the pathogenesis of PIH.
出处
《郑州大学学报(医学版)》
CAS
北大核心
2006年第1期68-70,共3页
Journal of Zhengzhou University(Medical Sciences)
基金
河南省自然科学基金资助项目0111022100