Evidence for direct CO2-mediated alterations in cerebral oxidative metabolism in humans
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Evidence for direct CO2-mediated alterations in cerebral oxidative metabolism in humans. / Caldwell, Hannah G.; Hoiland, Ryan L.; Bain, Anthony R.; Howe, Connor A.; Carr, Jay M.J.R.; Gibbons, Travis D.; Durrer, Cody G.; Tymko, Michael M.; Stacey, Benjamin S.; Bailey, Damian M.; Sekhon, Mypinder S.; MacLeod, David B.; Ainslie, Philip N.
In: Acta Physiologica, Vol. 240, No. 9, e14197, 2024.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Evidence for direct CO2-mediated alterations in cerebral oxidative metabolism in humans
AU - Caldwell, Hannah G.
AU - Hoiland, Ryan L.
AU - Bain, Anthony R.
AU - Howe, Connor A.
AU - Carr, Jay M.J.R.
AU - Gibbons, Travis D.
AU - Durrer, Cody G.
AU - Tymko, Michael M.
AU - Stacey, Benjamin S.
AU - Bailey, Damian M.
AU - Sekhon, Mypinder S.
AU - MacLeod, David B.
AU - Ainslie, Philip N.
N1 - Publisher Copyright: © 2024 The Author(s). Acta Physiologica published by John Wiley & Sons Ltd on behalf of Scandinavian Physiological Society.
PY - 2024
Y1 - 2024
N2 - Aim: How the cerebral metabolic rates of oxygen and glucose utilization (CMRO2 and CMRGlc, respectively) are affected by alterations in arterial PCO2 (PaCO2) is equivocal and therefore was the primary question of this study. Methods: This retrospective analysis involved pooled data from four separate studies, involving 41 healthy adults (35 males/6 females). Participants completed stepwise steady-state alterations in PaCO2 ranging between 30 and 60 mmHg. The CMRO2 and CMRGlc were assessed via the Fick approach (CBF × arterial-internal jugular venous difference of oxygen or glucose content, respectively) utilizing duplex ultrasound of the internal carotid artery and vertebral artery to calculate cerebral blood flow (CBF). Results: The CMRO2 was altered by 0.5 mL × min−1 (95% CI: −0.6 to −0.3) per mmHg change in PaCO2 (p < 0.001) which corresponded to a 9.8% (95% CI: −13.2 to −6.5) change in CMRO2 with a 9 mmHg change in PaCO2 (inclusive of hypo- and hypercapnia). The CMRGlc was reduced by 7.7% (95% CI: −15.4 to −0.08, p = 0.045; i.e., reduction in net glucose uptake) and the oxidative glucose index (ratio of oxygen to glucose uptake) was reduced by 5.6% (95% CI: −11.2 to 0.06, p = 0.049) with a + 9 mmHg increase in PaCO2. Conclusion: Collectively, the CMRO2 is altered by approximately 1% per mmHg change in PaCO2. Further, glucose is incompletely oxidized during hypercapnia, indicating reductions in CMRO2 are either met by compensatory increases in nonoxidative glucose metabolism or explained by a reduction in total energy production.
AB - Aim: How the cerebral metabolic rates of oxygen and glucose utilization (CMRO2 and CMRGlc, respectively) are affected by alterations in arterial PCO2 (PaCO2) is equivocal and therefore was the primary question of this study. Methods: This retrospective analysis involved pooled data from four separate studies, involving 41 healthy adults (35 males/6 females). Participants completed stepwise steady-state alterations in PaCO2 ranging between 30 and 60 mmHg. The CMRO2 and CMRGlc were assessed via the Fick approach (CBF × arterial-internal jugular venous difference of oxygen or glucose content, respectively) utilizing duplex ultrasound of the internal carotid artery and vertebral artery to calculate cerebral blood flow (CBF). Results: The CMRO2 was altered by 0.5 mL × min−1 (95% CI: −0.6 to −0.3) per mmHg change in PaCO2 (p < 0.001) which corresponded to a 9.8% (95% CI: −13.2 to −6.5) change in CMRO2 with a 9 mmHg change in PaCO2 (inclusive of hypo- and hypercapnia). The CMRGlc was reduced by 7.7% (95% CI: −15.4 to −0.08, p = 0.045; i.e., reduction in net glucose uptake) and the oxidative glucose index (ratio of oxygen to glucose uptake) was reduced by 5.6% (95% CI: −11.2 to 0.06, p = 0.049) with a + 9 mmHg increase in PaCO2. Conclusion: Collectively, the CMRO2 is altered by approximately 1% per mmHg change in PaCO2. Further, glucose is incompletely oxidized during hypercapnia, indicating reductions in CMRO2 are either met by compensatory increases in nonoxidative glucose metabolism or explained by a reduction in total energy production.
KW - blood flow
KW - carbon dioxide
KW - cerebral metabolic rate of oxygen
KW - Fick principle
KW - metabolism
KW - ultrasound
U2 - 10.1111/apha.14197
DO - 10.1111/apha.14197
M3 - Journal article
C2 - 38958262
AN - SCOPUS:85184443781
VL - 240
JO - Acta Physiologica
JF - Acta Physiologica
SN - 1748-1708
IS - 9
M1 - e14197
ER -
ID: 399234684