Placental Transmission of Atropine at Full-Term Pregnancy

Abstract

Measurements of placental transmission of atropine were performed during Caesarean section. Twenty-five patients received 3H-atropine 0.5 microgram . kg-1 i.v. 1-30 min before delivery. Maternal venous blood was sampled before the induction of anaesthesia and at the moment of delivery, together with umbilical arterial and venous blood. Total hydrogen-3 activity was determined by liquid scintillation counting. The stability of 3H-atropine was confirmed by paper chromatography. The concentrations in the umbilical vein 1 and 5 min after injection were respectively 12% and 93% of the corresponding maternal value. Those in the umbilical artery were approximately 50% of those in the umbilical vein during the same period.

Pharmacokinetic implications for the clinical use of atropine, scopolamine and glycopyrrolate

“…However, there were problems in following the blood levels of I4C with great accuracy in man (8), and different labelings gave different urinary excretion rates of atropine and its metabolites (9,10). In experimental clinical (11) and obstetrical (12,13) studies, "-atropine has been used but the measured radioactivity probably represented both intact atropine and its metabolites.…”

Neonatal cholinesterase inhibitor poisoning: Materno‐fetal exchange of pesticide

“…The placental transfer of atropine has been studied by several authors 6,7 . Atropine is rapidly transferred to the fetus after intravenous administration to the mother and impacts on the function of the fetal autonomic nervous system and therefore on the adaptation of the newborn 6,7 . Administration of atropine to the mother may cause a fetal tachycardia and lead to contraction of the uterus causing commencement of labour 1 .…”

Clonidine premedication reduces maternal requirement for intravenous morphine after cesarean delivery without affecting newborn's outcome

“…30 Our full-term fetuses and newborns showed no bradycardia in the 48 hours after delivery, but since cardiac output in fetuses and newborns is heavily dependent on HR, 24,26 it is important to know whether those exposed to maternal clonidine have a depressed HR response to atropine. It is reported that atropine rapidly crosses the placenta, with an F/M ratio of approximately 0.93 being attained at 5 min, 31 which eliminates short-term fetal HR variability. 31 The hypotension and bradycardia seen with clonidine are known to be principally due to the central effects of this drug (mediated by decreased sympathetic outflow), 8 and future studies will need to determine whether the responses to ephedrine and atropine are maintained in the fetus and newborn exposed to maternal clonidine.…”

“…It is reported that atropine rapidly crosses the placenta, with an F/M ratio of approximately 0.93 being attained at 5 min, 31 which eliminates short-term fetal HR variability. 31 The hypotension and bradycardia seen with clonidine are known to be principally due to the central effects of this drug (mediated by decreased sympathetic outflow), 8 and future studies will need to determine whether the responses to ephedrine and atropine are maintained in the fetus and newborn exposed to maternal clonidine.…”