DECREASED PROSTACYCLIN BIOSYNTHESIS PRECEDING THE CLINICAL MANIFESTATION OF PREGNANCY-INDUCED HYPERTENSION
DECREASED PROSTACYCLIN BIOSYNTHESIS PRECEDING THE CLINICAL MANIFESTATION OF PREGNANCY-INDUCED HYPERTENSION
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DOI:
10.1161/01.cir.75.5.956
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发表时间:
1987-05-01
期刊:
影响因子:
37.8
通讯作者:
FITZGERALD, GA
中科院分区:
文献类型:
--
作者:
FITZGERALD, DJ;ENTMAN, SS;FITZGERALD, GA
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.