Al M D, van Houwelingen A C, Badart-Smook A, Hasaart T H, Roumen F J, Hornstra G
Department of Human Biology, University of Limburg, Maastricht, The Netherlands.
Am J Obstet Gynecol. 1995 May;172(5):1605-14. doi: 10.1016/0002-9378(95)90505-7.
Our purpose was to investigate, in a prospective way, whether the altered essential fatty acid status observed in pregnancy-induced hypertension is a consequence of the disease or may contribute to its cause.
Pregnant women healthy at the start of the study were asked to give a blood sample before 16 weeks, at 22 weeks, and at 32 weeks of gestation. After delivery a blood sample from the umbilical vein, a piece of the umbilical cord, and a maternal blood sample were collected. Fatty acid compositions were determined of the phospholipids isolated from plasma and umbilical arterial and venous vessel walls. The nutrient intake of the pregnant women was assessed by use of the dietary history method and food frequency questionnaires. The results of each woman with pregnancy-induced hypertension were compared with the results of three matched healthy controls.
During pregnancy (16 to 32 weeks) no significant differences were observed in nutrient intake and maternal plasma fatty acid composition between the group with pregnancy-induced hypertension (n = 52) and the control group (n = 156). After delivery the relative amounts of 18:2(n-6) and 18:3(n-3) in maternal plasma were significantly lower in pregnancy-induced hypertension than in normal pregnancy. This was associated with significantly higher levels of (n-6) long-chain polyenes and cervonic acid (22:6[n-3]). In comparison with the situation at 32 weeks, the postpartum cervonic acid status increased in pregnancy-induced hypertension, whereas it decreased in normal pregnancy. The cervonic acid levels in umbilical plasma phospholipids were significantly higher after pregnancy-induced hypertension than after normal pregnancy. No significant differences were observed for the fatty acid content in umbilical vessel walls.
The results indicate that the altered essential fatty acid status in pregnancy-induced hypertension is a late phenomenon and is therefore unlikely to have contributed to the pathogenesis of pregnancy-induced hypertension. Moreover, the neonatal essential fatty acid status is not negatively affected by pregnancy-induced hypertension.
我们旨在前瞻性地研究,妊娠高血压综合征中观察到的必需脂肪酸状态改变是该疾病的结果还是可能导致其发病的原因。
选取研究开始时健康的孕妇,在妊娠16周前、22周和32周时采集血样。分娩后,采集脐静脉血样、一段脐带和母血样本。测定从血浆以及脐动脉和静脉血管壁中分离出的磷脂的脂肪酸组成。通过饮食史法和食物频率问卷评估孕妇的营养摄入情况。将每位妊娠高血压综合征患者的结果与三名匹配的健康对照者的结果进行比较。
在孕期(16至32周),妊娠高血压综合征组(n = 52)和对照组(n = 156)之间在营养摄入和母体血浆脂肪酸组成方面未观察到显著差异。分娩后,妊娠高血压综合征患者母体血浆中18:2(n - 6)和18:3(n - 3)的相对含量显著低于正常妊娠者。这与(n - 6)长链多烯和二十二碳六烯酸(22:6[n - 3])水平显著升高有关。与32周时的情况相比,妊娠高血压综合征患者产后二十二碳六烯酸状态升高,而正常妊娠者则降低。妊娠高血压综合征患者产后脐血浆磷脂中的二十二碳六烯酸水平显著高于正常妊娠者。脐血管壁中的脂肪酸含量未观察到显著差异。
结果表明,妊娠高血压综合征中必需脂肪酸状态的改变是一种晚期现象,因此不太可能导致妊娠高血压综合征的发病机制。此外,妊娠高血压综合征对新生儿必需脂肪酸状态没有负面影响。