Cerebral vasomotor reactivity: steady-state versus transient changes in carbon dioxide tension

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Abstract

New Findings

What is the central question of this study?

The relationship between changes in cerebral blood flow and arterial carbon dioxide tension is used to assess cerebrovascular function. Hypercapnia is generally evoked by two methods, i.e. steady-state and transient increases in carbon dioxide tension. In some cases, the hypercapnia is immediately preceded by a period of hypocapnia. It is unknown whether the cerebrovascular response differs between these methods and whether a period of hypocapnia blunts the subsequent response to hypercapnia.
What is the main finding and its importance?

The cerebrovascular response is similar between steady-state and transient hypercapnia. However, hyperventilation-induced hypocapnia attenuates the cerebral vasodilatory responses during a subsequent period of rebreathing-induced hypercapnia.

Cerebral vasomotor reactivity (CVMR) to changes in arterial carbon dioxide tension ( ) is assessed during steady-state or transient changes in . This study tested the following two hypotheses: (i) that CVMR during steady-state changes differs from that during transient changes in ; and (ii) that CVMR during rebreathing-induced hypercapnia would be blunted when preceded by a period of hyperventilation. For each hypothesis, end-tidal carbon dioxide tension ( ) middle cerebral artery blood velocity (CBFV), cerebrovascular conductance index (CVCI; CBFV/mean arterial pressure) and CVMR (slope of the linear regression between changes in CBFV and CVCI versus ) were assessed in eight individuals. To address the first hypothesis, measurements were made during the following two conditions (randomized): (i) steady-state increases in of 5 and 10 Torr above baseline; and (ii) rebreathing-induced transient breath-by-breath increases in . The linear regression for CBFV versus ( P = 0.65) and CVCI versus ( P = 0.44) was similar between methods; however, individual variability in CBFV or CVCI responses existed among subjects. To address the second hypothesis, the same measurements were made during the following two conditions (randomized): (i) immediately following a brief period of hypocapnia induced by hyperventilation for 1 min followed by rebreathing; and (ii) during rebreathing only. The slope of the linear regression for CBFV versus ( P < 0.01) and CVCI versus ( P < 0.01) was reduced during hyperventilation plus rebreathing relative to rebreathing only. These results indicate that cerebral vasomotor reactivity to changes in is similar regardless of the employed methodology to induce changes in and that hyperventilation-induced hypocapnia attenuates the cerebral vasodilatory responses during a subsequent period of rebreathing-induced hypercapnia.

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Most cited references 48

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Regional brain blood flow in man during acute changes in arterial blood gases.

A. Joe Shaw, N Eves, Frances J D Smith … (2012)

Despite the importance of blood flow on brainstem control of respiratory and autonomic function, little is known about regional cerebral blood flow (CBF) during changes in arterial blood gases.We quantified: (1) anterior and posterior CBF and reactivity through a wide range of steady-state changes in the partial pressures of CO2 (PaCO2) and O2 (PaO2) in arterial blood, and (2) determined if the internal carotid artery (ICA) and vertebral artery (VA) change diameter through the same range.We used near-concurrent vascular ultrasound measures of flow through the ICA and VA, and blood velocity in their downstream arteries (the middle (MCA) and posterior (PCA) cerebral arteries). Part A (n =16) examined iso-oxic changes in PaCO2, consisting of three hypocapnic stages (PaCO2 =∼15, ∼20 and ∼30 mmHg) and four hypercapnic stages (PaCO2 =∼50, ∼55, ∼60 and ∼65 mmHg). In Part B (n =10), during isocapnia, PaO2 was decreased to ∼60, ∼44, and ∼35 mmHg and increased to ∼320 mmHg and ∼430 mmHg. Stages lasted ∼15 min. Intra-arterial pressure was measured continuously; arterial blood gases were sampled at the end of each stage. There were three principal findings. (1) Regional reactivity: the VA reactivity to hypocapnia was larger than the ICA, MCA and PCA; hypercapnic reactivity was similar.With profound hypoxia (35 mmHg) the relative increase in VA flow was 50% greater than the other vessels. (2) Neck vessel diameters: changes in diameter (∼25%) of the ICA was positively related to changes in PaCO2 (R2, 0.63±0.26; P<0.05); VA diameter was unaltered in response to changed PaCO2 but yielded a diameter increase of +9% with severe hypoxia. (3) Intra- vs. extra-cerebral measures: MCA and PCA blood velocities yielded smaller reactivities and estimates of flow than VA and ICA flow. The findings respectively indicate: (1) disparate blood flow regulation to the brainstem and cortex; (2) cerebrovascular resistance is not solely modulated at the level of the arteriolar pial vessels; and (3) transcranial Doppler ultrasound may underestimate measurements of CBF during extreme hypoxia and/or hypercapnia.

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Integration of cerebrovascular CO2 reactivity and chemoreflex control of breathing: mechanisms of regulation, measurement, and interpretation.

James Duffin, Philip Ainslie (2009)

Cerebral blood flow (CBF) and its distribution are highly sensitive to changes in the partial pressure of arterial CO(2) (Pa(CO(2))). This physiological response, termed cerebrovascular CO(2) reactivity, is a vital homeostatic function that helps regulate and maintain central pH and, therefore, affects the respiratory central chemoreceptor stimulus. CBF increases with hypercapnia to wash out CO(2) from brain tissue, thereby attenuating the rise in central Pco(2), whereas hypocapnia causes cerebral vasoconstriction, which reduces CBF and attenuates the fall of brain tissue Pco(2). Cerebrovascular reactivity and ventilatory response to Pa(CO(2)) are therefore tightly linked, so that the regulation of CBF has an important role in stabilizing breathing during fluctuating levels of chemical stimuli. Indeed, recent reports indicate that cerebrovascular responsiveness to CO(2), primarily via its effects at the level of the central chemoreceptors, is an important determinant of eupneic and hypercapnic ventilatory responsiveness in otherwise healthy humans during wakefulness, sleep, and exercise and at high altitude. In particular, reductions in cerebrovascular responsiveness to CO(2) that provoke an increase in the gain of the chemoreflex control of breathing may underpin breathing instability during central sleep apnea in patients with congestive heart failure and on ascent to high altitude. In this review, we summarize the major factors that regulate CBF to emphasize the integrated mechanisms, in addition to Pa(CO(2)), that control CBF. We discuss in detail the assessment and interpretation of cerebrovascular reactivity to CO(2). Next, we provide a detailed update on the integration of the role of cerebrovascular CO(2) reactivity and CBF in regulation of chemoreflex control of breathing in health and disease. Finally, we describe the use of a newly developed steady-state modeling approach to examine the effects of changes in CBF on the chemoreflex control of breathing and suggest avenues for future research.

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The cerebrovascular response to carbon dioxide in humans.

Aaron J. Fisher, J Duffin, R A Battisti (2011)

Carbon dioxide (CO2) increases cerebral blood flow and arterial blood pressure. Cerebral blood flow increases not only due to the vasodilating effect of CO2 but also because of the increased perfusion pressure after autoregulation is exhausted. Our objective was to measure the responses of both middle cerebral artery velocity (MCAv) and mean arterial blood pressure (MAP) to CO2 in human subjects using Duffin-type isoxic rebreathing tests. Comparisons of isoxic hyperoxic with isoxic hypoxic tests enabled the effect of oxygen tension to be determined. During rebreathing the MCAv response to CO2 was sigmoidal below a discernible threshold CO2 tension, increasing from a hypocapnic minimum to a hypercapnic maximum. In most subjects this threshold corresponded with the CO2 tension at which MAP began to increase. Above this threshold both MCAv and MAP increased linearly with CO2 tension. The sigmoidal MCAv response was centred at a CO2 tension close to normal resting values (overall mean 36 mmHg). While hypoxia increased the hypercapnic maximum percentage increase in MCAv with CO2 (overall means from76.5 to 108%) it did not affect other sigmoid parameters. Hypoxia also did not alter the supra-threshold MCAv and MAP responses to CO2 (overall mean slopes 5.5% mmHg⁻¹ and 2.1 mmHg mmHg⁻¹, respectively), but did reduce the threshold (overall means from 51.5 to 46.8 mmHg). We concluded that in the MCAv response range below the threshold for the increase of MAP with CO2, the MCAv measurement reflects vascular reactivity to CO2 alone at a constant MAP.

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Author and article information

Journal

Journal ID (nlm-ta): Exp Physiol

Journal ID (iso-abbrev): Exp. Physiol

Journal ID (publisher-id): eph

Title: Experimental Physiology

Publisher: BlackWell Publishing Ltd (Oxford, UK )

ISSN (Print): 0958-0670

ISSN (Electronic): 1469-445X

Publication date (Print): 01 November 2014

Publication date (Electronic): 18 October 2014

Volume: 99

Issue: 11

Pages: 1499-1510

Affiliations

[1 ]Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital Dallas TX, USA

[2 ]Department of Internal Medicine, University of Texas Southwestern Medical Center Dallas, TX, USA

[3 ]Department of Kinesiology and Health Education, University of Texas at Austin TX, USA

Author notes

Corresponding author R. M. Brothers: Department of Kinesiology and Health Education, The University of Texas at Austin, Environmental and Autonomic Physiology Laboratory, 1 University Station: D-3700, Austin, TX 78712, USA. Email: r.m.brothers@ 123456mail.utexas.edu

Article

DOI: 10.1113/expphysiol.2014.081190

PMC ID: 4218865

PubMed ID: 25172891

SO-VID: 2fa534db-2350-4b38-ade9-29b30b92cece

License:

This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

Cerebral vasomotor reactivity: steady-state versus transient changes in carbon dioxide tension

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Abstract

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The Journal of Physiology

Most cited references 48

Regional brain blood flow in man during acute changes in arterial blood gases.

Integration of cerebrovascular CO2 reactivity and chemoreflex control of breathing: mechanisms of regulation, measurement, and interpretation.

The cerebrovascular response to carbon dioxide in humans.

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