AJP - Heart and Circulatory Physiology, Vol 265, Issue 1 9-14, Copyright © 1993 by American Physiological Society
Fetal responses to acute maternal cocaine injection in sheep
C. A. Gleason, H. Iida, T. P. O'Brien, M. D. Jones Jr, E. J. Cone and R. J. Traystman
Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore 21205.
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 pregnant sheep;
their fetuses had been catheterized in utero 2 days before the study. We
measured fetal cerebral blood flow (CBF), cerebral metabolic rate of O2
(CMRO2), mean arterial blood pressure (MAP), and blood gases before and 2,
5, 15, and 30 min after maternal cocaine injection. Fetal CBF increased by
37 +/- 33% (mean +/- SD) at 5 min and returned to baseline by 15 min.
Regional brain blood flow changes paralleled 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 unchanged for cerebral hemispheres and caudate.
Increased CBF at 5 min was associated with a 20 +/- 9% increase in fetal
MAP and a 38 +/- 13% decrease in fetal arterial O2 content. Fetal CMRO2 was
unchanged. There 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 in placental blood flow. Maternal cocaine injection causes fetal
hypoxemia, hypertension, and increased CBF. Possible mechanisms for
cerebral vasodilation (in some areas) include hypoxemia, impaired
autoregulatory response to increased blood pressure, and/or direct or
indirect vascular effects of cocaine or its metabolites.
