Effect of magnesium on fetal circulatory responses to acute hypoxemia

用“慢性制剂”山羊模型研究了硫酸镁对急性低氧血症胎儿循环反应的影响。急性低氧血症导致胎儿心率（FHR）减速与胎儿动脉血压（BP）的增加。低氧血症和持续镁输注掩盖了这些胎儿反应，FHR和血压没有变化。4小时镁输注可降低基线FHR、FHR加速发生率和基线变异性。急性低氧血症显著增加FHR变异，而镁不会减弱FHR变异。儿茶酚胺会因低氧血症以及含镁的低氧血症而增加。用彩色微球法测量血流量。从低氧血症前的水平来看，低氧血症显著增加了大脑皮层、中脑、小脑、髓质和心脏的血流量。镁进一步增加了流向这些器官的血液，这种流向大脑皮层的血液增加具有统计学意义。为了更好地了解镁的神经保护作用，我们采用7日龄大鼠模型（单侧颈动脉结扎，缺氧2小时）。缺氧缺血性损伤前镁预处理对脑各部位均有神经保护作用，但仅对大脑皮层有统计学意义。这些结果表明，镁对胎儿（和新生儿）有神经保护作用，镁增加流向大脑和心脏的血流量可能是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.