Abstract
We investigated the influence of arterial ( ) with and without acutely elevated arterial pH and bicarbonate ([HCO3- ]) on cerebral blood flow (CBF) regulation in the internal carotid artery and vertebral artery. We assessed stepwise iso-oxic alterations in (i.e. cerebrovascular CO2 reactivity) prior to and following i.v. sodium bicarbonate infusion (NaHCO3- ) to acutely elevate arterial pH and [HCO3- ]. Total CBF was unchanged irrespective of a higher arterial pH at each matched stage of , indicating that CBF is acutely regulated by rather than arterial pH. The cerebrovascular responses to changes in arterial H+ /pH were altered in keeping with the altered relationship between and H+ /pH following NaHCO3- infusion (i.e. changes in buffering capacity). Total CBF was ∼7% higher following NaHCO3- infusion during isocapnic breathing providing initial evidence for a direct vasodilatory influence of HCO3- independent of levels. Cerebral blood flow (CBF) regulation is dependent on the integrative relationship between arterial ( ), pH and cerebrovascular tone; however, pre-clinical studies indicate that intrinsic sensitivity to pH, independent of changes in or intravascular bicarbonate ([HCO3- ]), principally influences cerebrovascular tone. Eleven healthy males completed a standardized cerebrovascular CO2 reactivity (CVR) test utilizing radial artery catheterization and Duplex ultrasound (CBF); consisting of matched stepwise iso-oxic alterations in (hypocapnia: -5, -10mmHg; hypercapnia: +5, +10 mmHg) prior to and following i.v. sodium bicarbonate (NaHCO3- ; 8.4%, 50 mEq50mL-1 ) to elevate pH (7.408±0.020 vs. 7.461±0.030; P<0.001) and [HCO3- ] (26.1±1.4 vs. 29.3±0.9 mEqL-1 ; P<0.001). Absolute CBF was not different at each stage of CO2 reactivity (P=0.629) following NaHCO3- , irrespective of a higher pH (P<0.001) at each matched stage of (P=0.927). Neither hypocapnic (3.44±0.92 vs. 3.44±1.05% permmHg ; P=0.499), nor hypercapnic (7.45±1.85 vs. 6.37±2.23% permmHg ; P=0.151) reactivity to were altered pre- to post-NaHCO3- . When indexed against arterial [H+ ], the relative hypocapnic CVR was higher (P=0.019) and hypercapnic CVR was lower (P=0.025) following NaHCO3- , respectively. These changes in reactivity to [H+ ] were, however, explained by alterations in buffering between and arterial H+ /pH consequent to NaHCO3- . Lastly, CBF was higher (688±105 vs. 732±89 mLmin-1 , 7%±12%; P=0.047) following NaHCO3- during isocapnic breathing providing support for a direct influence of HCO3- on cerebrovascular tone independent of . These data indicate that in the setting of acute metabolic alkalosis, CBF is regulated by rather than arterial pH.
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