Arterial carbon dioxide and bicarbonate rather than pH regulate cerebral blood flow in the setting of acute experimental metabolic alkalosis
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Arterial carbon dioxide and bicarbonate rather than pH regulate cerebral blood flow in the setting of acute experimental metabolic alkalosis. / Caldwell, Hannah Grace; Howe, Connor A; Chalifoux, Carter J; Hoiland, Ryan L; Carr, Jay M J R; Brown, Courtney V; Patrician, Alexander; Tremblay, Joshua C; Panerai, Ronney B; Robinson, Thompson G; Minhas, Jatinder S; Ainslie, Philip N.
In: Journal of Physiology, Vol. 599, No. 5, 2021, p. 1439-1457.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Arterial carbon dioxide and bicarbonate rather than pH regulate cerebral blood flow in the setting of acute experimental metabolic alkalosis
AU - Caldwell, Hannah Grace
AU - Howe, Connor A
AU - Chalifoux, Carter J
AU - Hoiland, Ryan L
AU - Carr, Jay M J R
AU - Brown, Courtney V
AU - Patrician, Alexander
AU - Tremblay, Joshua C
AU - Panerai, Ronney B
AU - Robinson, Thompson G
AU - Minhas, Jatinder S
AU - Ainslie, Philip N
N1 - (Ekstern)
PY - 2021
Y1 - 2021
N2 - Cerebral blood flow (CBF) regulation is dependent on the integrative relationship between arterial PCO2 (PaCO2), pH and cerebrovascular tone; however, pre-clinical studies indicate that intrinsic sensitivity to pH, independent of changes in PaCO2 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 PaCO2 (hypocapnia: –5, –10 mmHg; hypercapnia: +5, +10 mmHg) prior to and following i.v. sodium bicarbonate (NaHCO3–; 8.4%, 50 mEq 50 mL–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 mEq L–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 PaCO2 (P = 0.927). Neither hypocapnic (3.44 ± 0.92 vs. 3.44 ± 1.05% per mmHg PaCO2; P = 0.499), nor hypercapnic (7.45 ± 1.85 vs. 6.37 ± 2.23% per mmHg PaCO2; P = 0.151) reactivity to PaCO2 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 PaCO2 and arterial H+/pH consequent to NaHCO3–. Lastly, CBF was higher (688 ± 105 vs. 732 ± 89 mL min–1, 7% ± 12%; P = 0.047) following NaHCO3– during isocapnic breathing providing support for a direct influence of HCO3– on cerebrovascular tone independent of PaCO2. These data indicate that in the setting of acute metabolic alkalosis, CBF is regulated by PaCO2 rather than arterial pH.
AB - Cerebral blood flow (CBF) regulation is dependent on the integrative relationship between arterial PCO2 (PaCO2), pH and cerebrovascular tone; however, pre-clinical studies indicate that intrinsic sensitivity to pH, independent of changes in PaCO2 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 PaCO2 (hypocapnia: –5, –10 mmHg; hypercapnia: +5, +10 mmHg) prior to and following i.v. sodium bicarbonate (NaHCO3–; 8.4%, 50 mEq 50 mL–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 mEq L–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 PaCO2 (P = 0.927). Neither hypocapnic (3.44 ± 0.92 vs. 3.44 ± 1.05% per mmHg PaCO2; P = 0.499), nor hypercapnic (7.45 ± 1.85 vs. 6.37 ± 2.23% per mmHg PaCO2; P = 0.151) reactivity to PaCO2 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 PaCO2 and arterial H+/pH consequent to NaHCO3–. Lastly, CBF was higher (688 ± 105 vs. 732 ± 89 mL min–1, 7% ± 12%; P = 0.047) following NaHCO3– during isocapnic breathing providing support for a direct influence of HCO3– on cerebrovascular tone independent of PaCO2. These data indicate that in the setting of acute metabolic alkalosis, CBF is regulated by PaCO2 rather than arterial pH.
KW - Acid–base balance
KW - Cerebral blood flow
KW - CO reactivity
KW - Metabolic alkalosis
KW - Sodium bicarbonate
UR - http://www.scopus.com/inward/record.url?scp=85099433566&partnerID=8YFLogxK
U2 - 10.1113/JP280682
DO - 10.1113/JP280682
M3 - Journal article
C2 - 33404065
AN - SCOPUS:85099433566
VL - 599
SP - 1439
EP - 1457
JO - The Journal of Physiology
JF - The Journal of Physiology
SN - 0022-3751
IS - 5
ER -
ID: 255835961