Ca. Gleason et al., FETAL RESPONSES TO ACUTE MATERNAL COCAINE INJECTION IN SHEEP, The American journal of physiology, 265(1), 1993, pp. 80000009-80000014
Maternal cocaine abuse has been associated with neonatal neurological
and neurobehavioral problems of unknown pathogenesis. We administered
a single intravenous dose of cocaine (2 mg/kg) to 12 unanesthetized pr
egnant sheep; their fetuses had been catheterized in utero 2 days befo
re the study. We measured fetal cerebral blood flow (CBF), cerebral me
tabolic rate of O2 (CMR(O2)), mean arterial blood pressure (MAP), and
blood gases before and 2, 5, 15, and 30 min after maternal cocaine inj
ection. Fetal CBF increased by 37 +/- 33% (mean +/- SD) at 5 min and r
eturned to baseline by 15 min. Regional brain blood flow changes paral
leled CBF changes with the greatest increases occurring in cerebellum
(54 +/- 43%) and brain stem (54 +/- 52%). Cerebral vascular resistance
was decreased for cerebellum (22%) and brain stem (19%) but was uncha
nged for cerebral hemispheres and caudate. Increased CBF at 5 min was
associated with a 20 +/- 9% increase in fetal MAP and a 38 +/- 13% dec
rease in fetal arterial O2 content. Fetal CMR(O2), was unchanged. Ther
e was a decrease in fetal intestinal blood flow at 2 min, an increase
in myocardial, adrenal, and renal blood flow at 5 min, and no change i
n placental blood flow. Maternal cocaine injection causes fetal hypoxe
mia, hypertension, and increased CBF. Possible mechanisms for cerebral
vasodilation (in some areas) include hypoxemia, impaired autoregulato
ry response to increased blood pressure, and/or direct or indirect vas
cular effects of cocaine or its metabolites.