Arterial carbon dioxide and bicarbonate rather than pH regulate cerebral blood flow in the setting of acute experimental metabolic alkalosis

Key points We investigated the influence of arterial () with and without acutely elevated pH bicarbonate ([HCO3–]) on cerebral blood flow (CBF) regulation in internal carotid artery vertebral artery. assessed stepwise iso-oxic alterations (i.e. cerebrovascular CO2 reactivity) prior to following i.v. sodium infusion (NaHCO3–) elevate [HCO3–]. Total CBF was unchanged irrespective a higher at each matched stage , indicating that is regulated by rather than pH. The responses changes H+/pH were altered keeping relationship between NaHCO3– buffering capacity). ?7% during isocapnic breathing providing initial evidence for direct vasodilatory HCO3– independent levels. Cerebral dependent integrative (), tone; however, pre-clinical studies indicate intrinsic sensitivity pH, or intravascular ([HCO3–]), principally influences tone. Eleven healthy males completed standardized reactivity (CVR) test utilizing radial catheterization Duplex ultrasound (CBF); consisting (hypocapnia: –5, –10 mmHg; hypercapnia: +5, +10 mmHg) (NaHCO3–; 8.4%, 50 mEq mL–1) (7.408 ± 0.020 vs. 7.461 0.030; P < 0.001) [HCO3–] (26.1 1.4 29.3 0.9 L–1; 0.001). Absolute not different (P = 0.629) NaHCO3–, 0.927). Neither hypocapnic (3.44 0.92 3.44 1.05% per mmHg ; 0.499), nor hypercapnic (7.45 1.85 6.37 2.23% 0.151) pre- post-NaHCO3–. When indexed against [H+], relative CVR 0.019) lower 0.025) respectively. These [H+] were, explained consequent NaHCO3–. Lastly, (688 105 732 89 mL min–1, 7% 12%; 0.047) support tone . data setting acute metabolic alkalosis,