American journal of obstetrics and gynecology
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Am. J. Obstet. Gynecol. · Jun 1979
Effects of magnesium sulfate treatment on perinatal calcium metabolism. I. Maternal and fetal responses.
Serial maternal and cord blood determinations of the ions and hormones involved in calcium homeostasis were made in pre-eclamptic women treated with intravenous magnesium sulfate. A 4 gm loading dose followed by 1 to 2 gm/hr caused maternal serum magnesium concentrations to rise 150%, to levels of 3.3 to 4.5 mEq/L, and ionized calcium levels to fall 16%, to 1.89 mEq/L. The hypocalcemia etly altering calcitonin. ⋯ At the time of delivery the offspring of these women were hypermagnesemic and relatively hypocalcemic, although less so than their mothers. Fetal ionized calcium levels, although lower with magnesium treatment than in control subjects, were within the lower limits of the normal range, which perhaps explains why the fetus did not respond with increased PTH or decreased calcitonin output. These results indicate that the principal maternal response to magnesium-induced hypocalcemia involves increased parathyroid hormone secretion which tends to preserve maternal calcium homeostasis, while the fetus is partially protected from hypermagnesemia and hypocalcemia by the placenta.
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Am. J. Obstet. Gynecol. · Jun 1979
Relationship of fetal bradycardia to maternal administration of lidocaine in sheep.
The casual relationship between the use of lidocaine and fetal bradycardia and the effect of the drug on maternal and fetal hemodynamics were studied on 13 chronically instrumented pregnant sheep. Lidocaine was infused intravenously to the mother for 60 minutes during arterial lidocaine concentrations were maintained at 2 to 5 microgram per milliliter in the mother and at less than 2 microgram per milliliter in the fetus. A decrease in uterine blood flow and an increase in uterine vascular resistance and uterine activity occurred immediately following the administration of lidocaine to the ewe. ⋯ These phenomena were seen in the absence of such predisposing conditions as maternal hypotension and fetal acidosis. It would appear that the mechanism responsible for a transient fetal bradycardia following regional obstetric anesthesia, particularly paracervical block anesthesia, in the initially nonasphyxiated fetus may in part be related to a brief decrease in perfusion of intervillous spaces. The bradycardia can occur at low lidocaine concentrations in both the maternal and fetal blood in a range similar to that observed in clinical practice.