ABSTRACT
BACKGROUND: Sodium bicarbonate (NaHCO3) is no longer recommended by the Neonatal Resuscitation Program (NRP), but is still being used by some neonatologists. The effects of NaHCO3 on cerebral hemodynamics are unclear. Therefore, we investigated the effects of NaHCO3 on cerebral blood flow (CBF) and cerebrovascular function using a newborn piglet model. METHODS: Newborn pigs were anesthetized, intubated, and ventilated. Cranial windows were implanted to evaluate changes in pial arteriolar diameters (PADs) as a surrogate for CBF during a 4-h intravenous infusion of 3% NaHCO3. Cerebrovascular reactivity to vasodilators and vasoconstrictors was investigated during vehicle control and during NaHCO3 infusion. RESULTS: NaHCO3 infusion caused significant and progressive pial arteriolar vasoconstrictions. During NaHCO3 infusion, cerebrovascular reactivity was preserved. Adding vasodilators decreased cerebral vasoconstriction, while adding vasoconstrictors exaggerated cerebral vasoconstriction. CONCLUSIONS: Intravenous infusion of NaHCO3 over 4 h caused progressive vasoconstriction of pial arterioles. Cerebrovascular function evaluated by the responses of pial arterioles to physiologically relevant vasoconstrictors and vasodilators was preserved during NaHCO3 infusion. A notable additional reduction of PADs was observed during NaHCO3 infusion in the presence of vasoconstrictors. Extrapolating our findings to human neonates should alarm the clinicians that using NaHCO3 in neonates may cause cerebral hypoperfusion. IMPACT: Cerebral vasoconstriction occurs during slow infusion of 3% diluted NaHCO3. Cerebral vasoconstriction is exaggerated when another vasoconstrictor is added during NaHCO3 infusion. Cerebrovascular function is preserved during NaHCO3 infusion. Clinicians should be aware of the risk of cerebral hypoperfusion with NaHCO3 infusion in vulnerable neonates.
