Cerebrovascular Effects of IV Dopamine Infusions in Preterm and Near-Term Fetal Sheep • 1870

Preterm infants often receive IV dopamine infusions after birth to maintain or increase their mean arterial blood pressure (MAP). One rationale for this therapeutic strategy is that reaching a “magic MAP” optimizes cerebral perfusion pressure and prevents brain injury. However, there is little data regarding cerebrovascular responses of the developing brain to IV dopamine. Using chronically-catheterized, unanesthetized fetal sheep, we tested the hypothesis that IV dopamine causes dosedependent cerebral vasoconstriction in immature fetuses. We measured catecholamine levels using an HPLC method, cerebral blood flow (CBF) via radiolabeled microspheres and cerebral arterial and venous (sagittal sinus) O₂ content, and we calculated cerebrovascular resistance (CVR = MAP ÷ CBF) and cerebral O₂ consumption (CMRO₂) and O₂ delivery (OD). We studied seven near-term (132 ± 1 days gestation) and eight preterm (93 ± 1 days) fetal sheep two days after vascular catheters were placed in utero. Measurements were made at baseline and at four dopamine infusion rates: 2.5, 7.5, 25 and 75 μg/kg/min. Results: (mean ± SEM) for higher doses: Table In addition, there was a dose-dependent increase in glucose and lactate concentrations, a decrease in arterial pH, but no significant changes in systemic or cerebral oxygenation or CMRO₂.

Table 1 No caption available.

Dopamine, at doses high enough to raise MAP at least 10% above baseline(preterm) and 29% above baseline (near-term), causes cerebral vasoconstriction. The pressor response is less but the cerebrovascular response is greater in preterm fetuses at lower dopamine concentration and could be detrimental to cerebral perfusion and O₂ delivery, particularly during hypoxia/ischemia.