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Dopamine does not limit fetal cerebrovascular responses to hypoxia

¹Division of Neonatology, Department of Pediatrics, University of Washington, Seattle, Washington; and ²Henry Medical Center and Piedmont Hospital, Atlanta, Georgia

Submitted 4 April 2006 ; accepted in final form 25 September 2006

Dopamine is used clinically to stabilize mean arterial blood pressure (MAP) in sick infants. One goal of this therapeutic intervention is to maintain adequate cerebral blood flow (CBF) and perfusion pressure. High-dose intravenous dopamine has been previously demonstrated to increase cerebrovascular resistance (CVR) in near-term fetal sheep. We hypothesized that this vascular response might limit cerebral vasodilatation during acute isocapnic hypoxia. We studied nine near-term chronically catheterized unanesthetized fetal sheep. Using radiolabeled microspheres to measure fetal CBF, we calculated CVR at baseline, during fetal hypoxia, and then with the addition of an intravenous dopamine infusion at 2.5, 7.5, and 25 µg·kg^–1·min^–1 while hypoxia continued. During acute isocapnic fetal hypoxia, CBF increased 73.0 ± 14.1% and CVR decreased 38.9 ± 4.9% from baseline. Dopamine infusion at 2.5 and 7.5 µg·kg^–1·min^–1, begun during hypoxia, did not alter CVR or MAP, but MAP increased when dopamine infusion was increased to 25 µg·kg^–1·min^–1. Dopamine did not alter CBF or affect the CBF response to hypoxia at any dose. However, CVR increased at a dopamine infusion rate of 25 µg·kg^–1·min^–1. This increase in CVR at the highest dopamine infusion rate is likely an autoregulatory response to the increase in MAP, similar to our previous findings. Therefore, in chronically catheterized unanesthetized near-term fetal sheep, dopamine does not alter the expected cerebrovascular responses to hypoxia.

cerebral blood flow; development; fetus