Cerebrovascular regulation during increases in systemic blood flow and systemic vascular resistance

It is unknown whether, under anesthesia, an increase in blood pressure by augmenting cardiac output would exert a different effect on brain perfusion compared with a rise in blood pressure by elevating systemic vascular resistance. In this study, we disentangled these two parameters by monitoring changes in middle cerebral artery blood velocity (MCA <i>V</i><sub>mean</sub>) and frontal cerebral lobe oxygenation (cO<sub>2</sub>Hb) in 15 patients on cardiopulmonary bypass (CPB) during two experiments. First, we increased systemic vascular resistance, using 100 μg phenylephrine, while CPB flow remained clamped. Second, we increased CPB flow while systemic vascular resistance remained unmodified. Mean arterial pressure increased 12 ± 4 mmHg and 11 ± 5 mmHg after raising systemic vascular resistance and cardiac blood flow, respectively (<i>P</i> = 0.60). Systemic vasoconstriction with a constant cardiac blood flow increased the MCA <i>V</i><sub>mean</sub> (17%, <i>P</i> = 0.001) while the cO<sub>2</sub>Hb declined (-2.2%, <i>P</i> = 0.005). Augmenting cardiac blood flow increased both MCA <i>V</i><sub>mean</sub> and cO<sub>2</sub>Hb (17%, <i>P</i> < 0.001, and 2.5%, <i>P</i> = 0.02) concordantly. Cerebral perfusion seemed to be dependent on cardiac blood flow, since both cO<sub>2</sub>Hb and MCA <i>V</i><sub>mean</sub> changed concordantly with an increase in cardiopulmonary bypass flow. A systemic vascular resistance-mediated blood pressure increase with the α<sub>1</sub>-adrenergic agonist phenylephrine had a comparable rise in MCA <i>V</i><sub>mean</sub> but a discordant effect on cO<sub>2</sub>Hb, presumably due to both cutaneous and cerebral vasoconstriction.<b>NEW & NOTEWORTHY</b> Elevating blood pressure by increasing cardiac blood flow ([Formula: see text]) or by increasing systemic vascular resistance (SVR) results in a comparable increase in middle cerebral artery blood velocity. In contrast, although frontal cerebral lobe oxygenation increased with increasing [Formula: see text], it decreased with increasing SVR. This difference was less pronounced when [Formula: see text] was kept constant, suggesting that part of the decrease may be attributed to an SVR-induced decrease in [Formula: see text].

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Publication Details

Journal
Journal of Applied Physiology
Published
2025-11-21
DOI
https://doi.org/10.1152/japplphysiol.00182.2025
Citations
1
Primary Topic
Traumatic Brain Injury and Neurovascular Disturbances
Type
article
Field-Weighted Citation Impact
1.39
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article

Cerebrovascular regulation during increases in systemic blood flow and systemic vascular resistance

Emma H.M. Torn, Bas van Zaane, Lisette M. Vernooij, Wilton A. van Klei et al.
1 citations
Journal of Applied Physiology
Traumatic Brain Injury and Neurovascular Disturbances
1.39
article

Cerebrovascular regulation during increases in systemic blood flow and systemic vascular resistance

Emma H.M. Torn, Bas van Zaane, Lisette M. Vernooij, Wilton A. van Klei, Rogier V. Immink, Jan-Folkert Heida, Niels P. van der Kaaij
article en
1 citations

Abstract

It is unknown whether, under anesthesia, an increase in blood pressure by augmenting cardiac output would exert a different effect on brain perfusion compared with a rise in blood pressure by elevating systemic vascular resistance. In this study, we disentangled these two parameters by monitoring changes in middle cerebral artery blood velocity (MCA <i>V</i><sub>mean</sub>) and frontal cerebral lobe oxygenation (cO<sub>2</sub>Hb) in 15 patients on cardiopulmonary bypass (CPB) during two experiments. First, we increased systemic vascular resistance, using 100 μg phenylephrine, while CPB flow remained clamped. Second, we increased CPB flow while systemic vascular resistance remained unmodified. Mean arterial pressure increased 12 ± 4 mmHg and 11 ± 5 mmHg after raising systemic vascular resistance and cardiac blood flow, respectively (<i>P</i> = 0.60). Systemic vasoconstriction with a constant cardiac blood flow increased the MCA <i>V</i><sub>mean</sub> (17%, <i>P</i> = 0.001) while the cO<sub>2</sub>Hb declined (-2.2%, <i>P</i> = 0.005). Augmenting cardiac blood flow increased both MCA <i>V</i><sub>mean</sub> and cO<sub>2</sub>Hb (17%, <i>P</i> < 0.001, and 2.5%, <i>P</i> = 0.02) concordantly. Cerebral perfusion seemed to be dependent on cardiac blood flow, since both cO<sub>2</sub>Hb and MCA <i>V</i><sub>mean</sub> changed concordantly with an increase in cardiopulmonary bypass flow. A systemic vascular resistance-mediated blood pressure increase with the α<sub>1</sub>-adrenergic agonist phenylephrine had a comparable rise in MCA <i>V</i><sub>mean</sub> but a discordant effect on cO<sub>2</sub>Hb, presumably due to both cutaneous and cerebral vasoconstriction.<b>NEW & NOTEWORTHY</b> Elevating blood pressure by increasing cardiac blood flow ([Formula: see text]) or by increasing systemic vascular resistance (SVR) results in a comparable increase in middle cerebral artery blood velocity. In contrast, although frontal cerebral lobe oxygenation increased with increasing [Formula: see text], it decreased with increasing SVR. This difference was less pronounced when [Formula: see text] was kept constant, suggesting that part of the decrease may be attributed to an SVR-induced decrease in [Formula: see text].

Journal of Applied PhysiologyVol. 139(6)
University Health Network (CA), University of Toronto (CA), Utrecht University (NL), Toronto General Hospital (CA), Health Net (US), University Medical Center Utrecht (NL), St. Antonius Ziekenhuis (NL), Amsterdam Neuroscience (NL), Amsterdam University Medical Centers (NL), Toronto General Hospital Research Institute, University of Amsterdam (NL)
Openalex Percentile: Top 14%
Traumatic Brain Injury and Neurovascular Disturbances
1.39
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