The effects of sodium bicarbonate infusion on cerebrovascular function in newborn pigs.

Abstract

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. 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. 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. 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. 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.