DECREASED PROSTACYCLIN BIOSYNTHESIS PRECEDING THE CLINICAL MANIFESTATION OF PREGNANCY-INDUCED HYPERTENSION

DECREASED PROSTACYCLIN BIOSYNTHESIS PRECEDING THE CLINICAL MANIFESTATION OF PREGNANCY-INDUCED HYPERTENSION
复制标题

DOI:
10.1161/01.cir.75.5.956
复制
发表时间:
1987-05-01
期刊:
影响因子:
37.8
通讯作者:
FITZGERALD, GA
FITZGERALD, GA
中科院分区:
医学1区
文献类型:
--
作者:
FITZGERALD, DJ;ENTMAN, SS;FITZGERALD, GA

文献摘要

被引文献

相似文献

与健康孕妇相比,妊娠高血压综合征患者的前列环素生物合成增加较少。目前尚不清楚这是否促进了临床疾病的发展,因此在妊娠高血压综合征的发病机制中可能是重要的,还是次要事件。我们使用非侵入性方法,通过测量尿代谢物2,3-二或-6-酮-前列腺素F1α,前瞻性地确定了有患妊娠高血压综合征风险的孕妇的前列环素生物合成。受试者是在怀孕不到20周时被招募的。分娩后,根据预先设定的标准将患者分为四组:(1)妊娠高血压综合征(n=12),(2)分娩时高血压(n=22),(3)慢性高血压(n=9),(4)正常血压(n=24)。在妊娠期,所有研究组的前列环素生物合成都显著增加。然而,发生妊娠高血压综合征的患者表现出较小的增量,并且这种差异在整个妊娠期间持续存在。这些结果与妊娠高血压综合征妇女前列环素生物合成改变的病理生理作用是一致的。此外,前列环素生成减少可确定有患妊娠高血压综合征风险的人群。这些信息将有助于阿司匹林等药物临床试验的设计,这些药物可能会阻止这种疾病的发展。
Patients who develop pregnancy-induced hypertension exhibit a lesser increment in prostacyclin biosynthesis than healthy pregnant subjects. Whether this precided the development of clinical disease and therefore may be important in the pathogenesis of pregnancy-induced hypertension or is a secondary event is unknown. We prospectively determined prostacyclin biosynthesis in pregnant subjects at risk of developing pregnancy-induced hypertension by use of noninvasive approach, measurement of the urinary metabolite 2,3-dinor-6-keto-prostaglandin F1.alpha.. Patients were recruited at less than 20 weeks gestation. After delivery, patients were retrospectively allocated by use of preset criteria, to one of four groups: (1) pregnancy-induced hypertension (n = 12), (2) hypertension in labor (n = 22), (3) chronic hypertension (n = 9), and (4) normotension (n = 24). There was a significant increase in prostacyclin biosynthesis in all study groups during gestation. However, patients who developed pregnancy-induced hypertension exhibited a lesser increment and this difference persisted throughout gestation. These results are consistent with a pathophysiologic role for altered prostacyclin biosynthesis in women with pregnancy-induced hypertension. In addition, decreased prostacyclin formation identifies a population at risk of developing pregnancy-induced hypertension. Such information would assist the design of clinical trials of drugs, such as aspirin, that might prevent the development of this disease.