Shun Yasuda1, Hyo Kyozuka1, Yasuhisa Nomura2, Keiya Fujimori1. 1. Department of Obstetrics and Gynecology, Fukushima Medical University, Fukushima, Japan. 2. Department of Obstetrics and Gynecology, Ohta Nishinouchi Hospital, Koriyama, Japan.
Abstract
AIM: To investigate the effects of magnesium sulfate on fetal baroreflex in normoxemia or acute fetal hypoxemia. METHODS: Fetal baroreflex response was elicited using phenylephrine (30 μg) in saline and magnesium sulfate in 8 chronically treated and instrumented fetal sheep. Hypoxemia was induced using nitrogen gas inflow for 30 min. Baroreflex, calculated as the ratio of the fetal heart rate change to the mean arterial pressure, was monitored after magnesium sulfate administration and in rapid and nonrapid eye movement (NREM) sleep states. Baroreflex was assessed in response to hypoxemia in control groups in both the rapid and NREM sleep states. RESULTS: Baroreflex was not significantly affected by saline, magnesium sulfate and rapid or NREM sleep states in normoxemic sheep. Hypoxemia increased the baroreflex in the saline-treated group (hypoxemic vs normoxemic rapid eye movement sleep: 4.37 ± 2.48 vs 2.72 ± 0.83; P < 0.05; hypoxemic vs normoxemic NREM sleep: 4.30 ± 1.47 vs 3.15 ± 0.83; P < 0.001). Magnesium sulfate decreased the baroreflex in the hypoxemic fetuses (magnesium sulfate hypoxemic vs. control normoxemic fetuses: 1.42 ± 0.92 vs 3.15 ± 0.83, P < 0.05). CONCLUSION: The hypoxemic fetal sheep, from the ewes that were receiving magnesium sulfate, showed a significantly reduced in the baroreflex response. In clinical practice, baroreflex-related decelerations in hypoxemic fetuses of mothers receiving magnesium sulfate should be carefully interpreted.
AIM: To investigate the effects of magnesium sulfate on fetal baroreflex in normoxemia or acute fetal hypoxemia. METHODS: Fetal baroreflex response was elicited using phenylephrine (30 μg) in saline and magnesium sulfate in 8 chronically treated and instrumented fetal sheep. Hypoxemia was induced using nitrogen gas inflow for 30 min. Baroreflex, calculated as the ratio of the fetal heart rate change to the mean arterial pressure, was monitored after magnesium sulfate administration and in rapid and nonrapid eye movement (NREM) sleep states. Baroreflex was assessed in response to hypoxemia in control groups in both the rapid and NREM sleep states. RESULTS: Baroreflex was not significantly affected by saline, magnesium sulfate and rapid or NREM sleep states in normoxemic sheep. Hypoxemia increased the baroreflex in the saline-treated group (hypoxemic vs normoxemic rapid eye movement sleep: 4.37 ± 2.48 vs 2.72 ± 0.83; P < 0.05; hypoxemic vs normoxemic NREM sleep: 4.30 ± 1.47 vs 3.15 ± 0.83; P < 0.001). Magnesium sulfate decreased the baroreflex in the hypoxemic fetuses (magnesium sulfate hypoxemic vs. control normoxemic fetuses: 1.42 ± 0.92 vs 3.15 ± 0.83, P < 0.05). CONCLUSION: The hypoxemic fetal sheep, from the ewes that were receiving magnesium sulfate, showed a significantly reduced in the baroreflex response. In clinical practice, baroreflex-related decelerations in hypoxemic fetuses of mothers receiving magnesium sulfate should be carefully interpreted.