Effect of magnesium on fetal circulatory responses to acute hypoxemia

采用“慢性准备”山羊模型，研究了硫酸镁对急性低氧血症时胎儿循环反应的影响。急性低氧血症导致胎儿心率减慢，胎儿动脉压升高。持续输注镁的低氧血症掩盖了这些胎儿的反应，FHR或BP没有变化。输镁4小时可降低基线FHR、FHR加速的发生率和基线变异性。急性低氧血症显著增加FHR的变异性，这种变化不会因镁而变钝。儿茶酚胺在低氧血症和低氧镁血症时增加。血流量用彩色微球法测量。从低氧前水平来看，低氧血症显著增加了流向大脑皮层、中脑、小脑、髓质和心脏的血流量。为了更好地了解镁的神经保护作用，我们采用7日龄大鼠(单侧颈动脉结扎低氧2小时)模型。在缺氧缺血性损伤前给予镁的预处理对大脑的各个部位都有神经保护作用，但统计学意义仅限于大脑皮层。这些结果表明镁对胎儿(和新生儿)具有神经保护作用，镁增加了流向大脑和心脏的血液可能是其神经保护作用的原因。

Effect of magnesium sulfate on fetal circulatory responses to acute hypoxemia was studied with a "chronic preparation" goat model.Acute hypoxemia causes fetal heart rate (FHR) deceleration with an increase in fetal arterial blood pressure (BP). Hypoxemia with a continuous magnesium infusion masks these fetal responses and shows no changes in FHR or BP.Four-hours magnesium infusion decreases baseline FHR, incidence of acceleration of FHR, and baseline variabilities. Acute hypoxemia significantly increases FHR variabilities, which are not blunted by magnesium. Catecholamines are increased by hypoxemia as well as hypoxemia with magnesium.Blood flow is measured by a colored microsphere method. From the pre-hypoxemic level, hypoxemia significantly increases blood flow to the cerebral cortex, midbrain, cerebellum, medulla, and heart. Magnesium further increases blood low to these organs, and this increase to the cerebral cortex achieves statistical significance.To better understand magnesium neuroprotective effect, we use 7-day-old rats model (unilateral carotid artery ligation with 2 hours hypoxia). Pretreatment of magnesium before the hypoxic-ischemic insult shows neuroprotective effects in all the part of the brain, but statistical significance is limited to the cerebral cortex.These results reveal that magnesium has neuroprotective effects on the fetus (and newborn), and that increases in blood flow to the brain and heart with magnesium may account for the neuroprotective effects.