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Magnesium sulfate exposure increases fetal blood flow redistribution to the brain during acute non-acidemic hypoxemia in goats.

Early Human Development

Anoxia, chemically induced, physiopathology, Blood Gas Analysis, Blood Pressure, drug effects, Brain, blood supply, embryology, Female, Fetal Blood, Goats, blood, Heart Rate, Fetal, Hydrogen-Ion Concentration, Magnesium Sulfate, pharmacology, Maternal-Fetal Exchange, Nitrogen, Pregnancy, Regional Blood Flow, Animals

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      It is still controversial that intrapartum exposure to magnesium may or may not reduce brain damage in premature infants in human and animal models. We investigated the effect of hypoxemia alone under magnesium exposure on fetal cardiovascular changes in chronically catheterized goat fetuses. We performed a 3-day experimental protocol with control (10% glucose) on day 1, recovery on day 2, and magnesium on day 3. Magnesium sulfate was directly infused to fetuses in a bolus dose of 270 mg/kg followed by 80 mg/kg/h. Hypoxemia was induced by maternal inhalation of nitrogen gas on day 1 and on day 3. Cerebral blood flow was measured by colored microsphere techniques. Repeated measure ANOVA and Bonferroni's/Dunn's test were used for comparison. Six Japanese Saanen goats at 0.85 gestation. Fetal heart rate, blood pressure, and cerebral blood flow. Ionized magnesium concentrations were significantly increased. Fetal PO2 decreased significantly from 30 mmHg to 14 mmHg without acidemia. Magnesium exposure significantly attenuated hypoxemia-induced bradycardia but did not affect blood pressure. Hypoxemia significantly increased fetal brain blood flow from the pre-hypoxic levels on day 1. Magnesium exposure further increased hypoxemia-induced brain blood flow on day 3, but statistical significance was limited to the cerebral cortex. In near-term, initially healthy goat fetuses, brain blood flow during acute hypoxemia was significantly increased with magnesium sulfate exposure.

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