[怀孕期间钙离子载体激活的中性粒细胞白三烯B4释放的定量变化-正常妊娠和子痫前期]。

Nihon Sanka Fujinka Gakkai zasshi Pub Date : 1996-06-01
T Imai, T Arai
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引用次数: 0

摘要

通过测定钙离子载体活化的中性粒细胞释放白三烯B4 (LTB4)的量,探讨正常妊娠期间中性粒细胞功能的变化以及正常孕妇与子痫前期妇女中性粒细胞功能的差异。此外,我们还检测了正常孕妇中性粒细胞磷脂的花生四烯酸(AA)含量和脂肪酸组成。在正常妊娠中,LTB4的释放量随妊娠显著下降。在子痫前期妇女中,LTB4的释放量明显高于正常妊娠妇女,但与非妊娠妇女无显著差异。正常孕妇AA含量随妊娠期明显降低。其他脂肪酸组成方面,随着妊娠,饱和脂肪酸增加,不饱和脂肪酸减少。结果表明,与非孕妇相比,孕妇的LTB4释放受到更大的抑制,孕妇的AA含量也有所下降。此外,脂肪酸组成的变化显示出细胞膜流动性下降的迹象。这一现象被认为是由于抑制中性粒细胞激活的机制伴随着LTB4释放量的减少。相反,在子痫前期妇女中没有观察到类似的抑制作用,这种机制的失败似乎有助于子痫前期的发展。
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[Quantitative changes in leukotriene B4 release in neutrophilic leukocytes activated by Ca ionophore during pregnancy--normal pregnancy and preeclampsia].

The amount of Leukotriene B4 (LTB4) released from neutrophilic leukocyte activated by calcium ionophore was measured to examine neutrophilic functions regarding the changes during normal pregnancy and differences between normal pregnant women and preeclamptic women. In addition, we examined the arachidonic acid (AA) content and fatty acid composition of neutrophilic phospholipid in normal pregnant women. In a normal pregnancy, the amount of LTB4 released decreased significantly with gestation. In preeclamptic women, the amount of LTB4 released was significantly higher than that in normal pregnant women, but there was no significant difference from non-pregnant women. Normal pregnant women showed a significantly decreased AA content with gestation. Regarding other fatty acids, as to fatty acid composition, there was increased saturated fatty acid and decreased unsaturated fatty acid with gestation. The results suggested that the LTB4 released was inhibited more in pregnant women than in non-pregnant women, and pregnant women also had decreased AA content. In addition, changes in fatty acid compositions showed signs of decreased fluidity of the cell membrane. This phenomenon is thought to be due to a mechanism to inhibiting the activation of neutrophilic leukocytes accompanied by a decrease in the amount of LTB4 released. Conversely, no similar inhibition was observed in preeclamptic women, and the failure of this mechanism seemed to contribute to the development of preeclampsia.

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