PROSTACYCLIN PRODUCTION DURING PREGNANCY - COMPARISON OF PRODUCTION DURING NORMAL-PREGNANCY AND PREGNANCY COMPLICATED BY HYPERTENSION
PROSTACYCLIN PRODUCTION DURING PREGNANCY - COMPARISON OF PRODUCTION DURING NORMAL-PREGNANCY AND PREGNANCY COMPLICATED BY HYPERTENSION
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DOI：
10.1016/s0002-9378(16)32525-x
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发表时间：
1982-01-01
影响因子：
9.8
通讯作者：
BRANCH, RA
中科院分区：
文献类型：
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作者：
GOODMAN, RP;KILLAM, AP;BRANCH, RA
通过测量2，3-二去甲-6-酮-前列腺素F1 α的尿排泄来研究妊娠期间前列环素（PGI 2）的生物合成。（地诺）和15-酮基-13，14-二氢-2，3-地诺-6-酮基-前列腺素F1 α。(15 KD DINOR），使用特定的气相色谱-质谱测定法。9名血压正常的非妊娠妇女、5名妊娠中期血压正常的妇女、8名妊娠晚期血压正常的妇女和6名妊娠晚期发生高血压的妇女提供了24小时尿样。正常妊娠妇女尿中dinor排泄量比非妊娠妇女增加5倍（253 . ±.对照组为21 ng dinor/g肌酐，对照组为1224 ±。110和1127 .+-.第二和第三孕期为152例）（平均值±。SEM [平均值的标准误差]）。与血压正常的孕妇受试者相比，患有高血压的孕妇受试者的尿dinor排泄显著减少（50%）（561 ± 0.001）。105 ng dinor/g肌酐）。在从每组中选择的受试者中，地诺与15 kd地诺的比例保持恒定。PGI 2的生物合成在正常妊娠期间增加，而这种增加在妊娠高血压中较少。这增加了PGI 2在正常妊娠期间有助于介导血流动力学变化的可能性，并且生产的相对减少可能与妊娠高血压的发病机制有关。
Prostacyclin (PGI2) biosynthesis during pregnancy was investigated by measuring urinary excretion of 2,3-dinor-6-keto-prostaglandin F1.alpha. (dinor) and 15-keto-13,14-dihydro-2,3-dinor-6-keto-prostaglandin F1.alpha. (15 kd dinor) with the use of specific gas chromatography-mass spectometry assays. Nine normotensive nonpregnant women, 5 normotensive women in the mid-trimester of pregnancy, 8 normotensive women in the 3rd trimester of pregnancy and 6 women who developed hypertension during the 3rd trimester provided 24-h samples of urine. Normal pregnant women had a 5-fold increase in urinary excretion of dinor in comparison to nonpregnant women (253 .+-. 21 ng dinor/g creatinine for controls vs. 1224 .+-. 110 and 1127 .+-. 152 for 2nd and 3rd trimesters) (mean .+-. SEM [standard error of the mean]). Pregnant subjects with hypertension had a significant (50%) reduction in urinary dinor excretion in comparison to normotensive pregnant subjects (561 .+-. 105 ng dinor/g creatinine). In subjects selected from each group, the ratio of dinor to 15 kd dinor remained constant. PGI2 biosynthesis is increased during normal pregnancy, and this increase is less in pregnancy-induced hypertension. This raises the possibility that PGI2 helps mediate hemodynamic changes during normal pregnancy, and that a relative decrease in production might be related to the pathogenesis of pregnancy-induced hypertension.