JAMA · 1987 · 513 citations · 12 references
MedicineObstetricsPharmacologyDevelopmental ToxicologyMaternal-fetal MedicineReproductive PhysiologyFetal DistressFetal PhysiologyMaternal-fetal PhysiologyPregnancyPregnancy PhysiologyPrenatal DevelopmentArterial Blood Gas AssessmentArterial Blood Gas SamplingBlood FlowBlood PressureFetal Adaptation To HypoxiaFetal Cardiovascular DevelopmentMaternal Cardiovascular ResponseMaternal Hemodynamic Effects On Fetal Status
In a controlled study, five pregnant ewes and their singleton fetuses were instrumented at 115–120 days gestation to record cardiovascular parameters and uterine blood flow, and cocaine was administered intravenously to the ewe or fetus (0.5–2.0 mg kg⁻¹) with measurements taken for 60 min. Maternal cocaine produced dose‑dependent hypertension and a 52–168 % rise in uterine vascular resistance, reducing uterine blood flow and causing fetal hypoxemia, hypertension, and tachycardia; fetal injection elicited smaller cardiovascular changes and no arterial blood‑gas alterations, indicating that cocaine impairs fetal oxygenation via uterine blood flow reduction and may trigger fetal catecholamine responses. JAMA 1987;257:957‑961.
Five pregnant ewes and their singleton fetuses were instrumented at 115 to 120 days' gestation (term, 145 days) for heart rate, blood pressure, uterine blood flow, and arterial blood gas sampling. In separate studies, cocaine was given to the ewe or fetus as a 0.5-, 1.0-, or 2.0-mg/kg intravenous bolus, and cardiovascular and arterial blood gas values were obtained for 60 minutes after the injection. The results showed that maternal administration of cocaine produced dose-dependent increases in maternal blood pressure and decreases in uterine blood flow. Uterine vascular resistance increased by 52%, 96%, and 168%, respectively. These responses were accompanied by marked fetal hypoxemia, hypertension, and tachycardia. Direct cocaine administration to the fetus produced smaller increases in fetal heart rate and blood pressure than those observed following maternal cocaine injection, and no significant changes in fetal arterial blood gas values. The conclusions are (1) cocaine alters fetal oxygenation by reducing uterine blood flow and impairing oxygen transfer to the fetus; and (2) fetal cardiovascular changes to maternal administration of cocaine may reflect fetal hypoxemia, increased fetal levels of cocaine or fetal catecholamines, or a combination of these events. (<i>JAMA</i>1987;257:957-961)
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David Acker, Benjamin P. Sachs, Kevin J. Tracey et al. · American Journal of Obstetrics and Gynecology · 1983 · 228 citations
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