REGULATION OF PLACENTAL VASCULAR REACTIVITY IN PIH

妊娠高血压综合征(PIH)与 可能由以下原因引起的胎儿和新生儿发病率和死亡率 宫内缺氧。妊高征的主要病理表现为 子宫胎盘血流量减少，但现代成像 技术人员现在表明，胎儿阻抗的增加- 胎盘循环和血流量减少也可能是 在妊高征中被发现。这可能代表了缺氧或BE的直接影响 胎儿适应增加胎盘吸氧至 缓解缺氧。胎儿-胎盘循环是由 体液因子和血管压力。不平衡的 血管扩张剂前列环素(PGI2)与血管收缩因子血栓素 据报道，(TXA2)的产生是血管收缩的基础 在妊高征中见过。 我们将从一个前提开始，即存在 PGI2、TXA2在妊高征发病中的作用我们将在胎儿胎盘中建立 人胎盘子叶灌流后的血液循环 血压正常和妊高征孕妇： 1.如果PGI2/TXA2的产生存在这种不平衡 2.其与胎儿胎盘反应的关系 循环至血管收缩 3.增加胎盘血流量对PGI2的影响 血管紧张剂的产生和反应。 4.低钙、低镁血症对前列环素的影响 合成和补充这些阳离子是否会改变 对血管收缩药的反应 5.如果缺氧减少了PGI2的合成或血管紧张素转换 酶活性和So改变血管反应性 6.脂氧合酶产物是否增加 (白三烯)的形成与PGI2合成不足有关 7.如果现在使用药物来恢复妊高征患者的PGI2/TXA2平衡 可能会穿过胎盘，改变脐带血管的反应性。 我们的主要目标是阐明潜在的作用和 PGI2/TXA2失衡在血管控制中的作用 胎儿/胎盘循环的反应性，潜在的 PGI2/TXA2失衡背后的机制及其原因 治疗药物可能会影响这一点，以改善血液流动和 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.