REGULATION OF PLACENTAL VASCULAR REACTIVITY IN PIH

妊娠高血压综合征（PIH）与妊娠高血压相关。 胎儿和新生儿的发病率和死亡率可能由 子宫内缺氧 妊高征的主要病理包括 子宫胎盘血流减少，但现代成像 技术人员现在已经表明，胎儿的阻抗增加， 胎盘循环和因此减少的血流量也可以 在PIH中发现 这可能是缺氧的直接影响， 胎儿适应性增加胎盘氧摄取， 缓解缺氧。 胎儿-胎盘循环由 体液因子和血管压力。 的不平衡 血管扩张剂前列环素（PGI 2）和血管收缩剂血栓素 据报道，血栓素A2（TxA 2）的产生是血管收缩的基础。 在PIH中看到 我们将从这样一个前提开始： 妊高征患者PGI_2和TxA_2的变化。 我们将在胎儿胎盘中建立 人胎盘子叶的血液循环 正常血压和PIH妊娠： 1. 如果PGI 2/TxA 2产生存在这种不平衡， 2. 其与胎儿-胎盘反应的关系 血管收缩剂循环 3. 增加胎儿-胎盘血流对PGI_2的影响 产生和对血管收缩剂的反应。 4. 低钙、低镁血症对前列环素的影响 合成，如果补充这些阳离子改变 对血管收缩剂的反应 5. 如果缺氧减少PGI 2合成或血管紧张素转换 酶活性，从而改变血管反应性 6. 脂氧合酶产物是否增加 （白三烯）形成与PGI 2合成缺陷有关 7. 如果现在使用药物来恢复PIH中的PGI 2/TxA 2平衡， 可能穿过胎盘并改变脐血管反应性。 我们的主要目标是阐明潜在的作用， PGI_2/TxA_2的失衡可能在控制血管紧张素转换酶活性方面起着重要作用。 胎儿/胎盘循环的反应性， PGI 2/TxA 2失衡背后的机制以及如何 治疗剂可以影响这一点以改善血流， 降低胎儿发病率和死亡率。

Pregnancy-induced hypertension (PIH) is associated with increased fetal and neonatal morbidity and mortality possibly resulting from hypoxia in utero. The primary pathology of PIH involves a reduction in uteroplacental blood flow but modern imaging techiques have now shown that increased impedance of the fetal- placental circulation and hence reduced blood flow can also be found in PIH. This may represent a direct effect of hypoxia or be a fetal adaptation to increase placental oxygen extraction to relieve hypoxia. The fetal-placental circulation is regulated by humoral agents and vascular pressure. An imbalance of vasodilator prostacyclin (PGI2) and vasoconstrictor thromboxane (TxA2) production is reported to underlie the vasoconstriction seen in PIH. We will commence with the premise that there is an imbalance of PGI2 and TxA2 in PIH. We will establish in the fetal-placental circulation of the perfused human placental cotyledon from both normotensive and PIH pregnancies: 1. If such an imbalance in PGI2/TxA2 production exists 2. Its relationship to the responses of the fetal-placental circulation to vasoconstrictors 3. The effect of increasing fetal-placental flow on PGI2 production and responses to vasoconstrictors. 4. The effects of hypocalcemia and hypomagnesemia on PGI2 synthesis and if supplementation with these cations alters responses to vasoconstrictors 5. If hypoxia reduces PGI2 synthesis or angiotensin converting enzyme activity and so alters vascular reactivity 6. Whether there is an increase in lipoxygenase product (leukotriene) formation linked to the deficiency in PGI2 synthesis 7. If drugs now used to restore the PGI2/TxA2 balance in PIH may cross the placenta and alter umbilical vascular reactivity. Our primary objective is to elucidate the potential role an imbalance in PGI2/TxA2 may have in controlling the vascular reactivity of the fetal/placental circulation, what the underlying mechanisms are behind the PGI2/TxA2 imbalance and how therapeutic agents may affect this to improve blood flow and reduce fetal morbidity and mortality.