Intravenous clonidine hydrochloride toxicity in pregnant ewes
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SummaryAdministration of intravenous clonidine hydrochloride has been advocated to rapidly control blood pressure in severe preeclampsia. To examine clonidine's acute maternal and fetal effects we intravenously injected 300 μg clonidine in eight chronically prepared normotensive near term ewes. Unlike intravenous saline solution injection, clonidine produced significant toxicity-intraamniotic pressure increased 97 ± 27% (p < 0.05), uterine blood flow decreased 55 ± 7% (p < 0.001), maternal and fetal serum glucose increased 158 ± 23% and 249 ± 91%, respectively (p < 0.001), and maternal and fetal PO2 decreased to 44 mm Hg ± 4 mm Hg and 13 mm Hg ± 1 mm Hg, respectively (p < 0.05). Maternal and fetal blood pressure and serum Cortisol were unaffected by clonidine, whereas heart rate decreased. No adverse maternal or fetal effects were noted with serum clonidine concentrations < 1.0 ng/ml. Direct fetal infusion of clonidine did not lower fetal arterial PO2 levels, although heart rates decreased and serum glucose levels increased. The multiple effects of clonidine infusion are best explained by actions on α2-adrenergic receptors. These results suggest that intravenous administration of clonidine may adversely affect the fetus by direct actions and by alterations in maternal physiology. (Am J Obstet Gynecol 1988;160:471-6.)

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