Dynamic Cerebral Autoregulation Changes during Sub-Maximal Handgrip Maneuver

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Abstract

Purpose

We investigated the effect of handgrip (HG) maneuver on time-varying estimates of dynamic cerebral autoregulation (CA) using the autoregressive moving average technique.

Methods

Twelve healthy subjects were recruited to perform HG maneuver during 3 minutes with 30% of maximum contraction force. Cerebral blood flow velocity, end-tidal CO ₂ pressure (PETCO ₂), and noninvasive arterial blood pressure (ABP) were continuously recorded during baseline, HG and recovery. Critical closing pressure (CrCP), resistance area-product (RAP), and time-varying autoregulation index (ARI) were obtained.

Results

PETCO ₂ did not show significant changes during HG maneuver. Whilst ABP increased continuously during the maneuver, to 27% above its baseline value, CBFV raised to a plateau approximately 15% above baseline. This was sustained by a parallel increase in RAP, suggestive of myogenic vasoconstriction, and a reduction in CrCP that could be associated with metabolic vasodilation. The time-varying ARI index dropped at the beginning and end of the maneuver (p<0.005), which could be related to corresponding alert reactions or to different time constants of the myogenic, metabolic and/or neurogenic mechanisms.

Conclusion

Changes in dynamic CA during HG suggest a complex interplay of regulatory mechanisms during static exercise that should be considered when assessing the determinants of cerebral blood flow and metabolism.

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Most cited references 30

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Comparison of static and dynamic cerebral autoregulation measurements.

Peter D. Newell, Wilbur Lam, F P Tiecks … (1995)

Cerebral autoregulation can be evaluated by measuring relative blood flow changes in response to a steady-state change in the blood pressure (static method) or during the response to a rapid change in blood pressure (dynamic method). The purpose of this study was to compare the results of the two methods in humans with both intact and impaired autoregulatory capacity. Using intraoperative transcranial Doppler sonography recordings from both middle cerebral arteries, we determined static and dynamic autoregulatory responses in 10 normal subjects undergoing elective surgical procedures. The changes in cerebrovascular resistance were estimated from the changes in cerebral blood flow velocity and arterial blood pressure in response to manipulations of blood pressure. Static autoregulation was determined by analyzing the response to a phenylephrine-induced rise in blood pressure, whereas rapid deflation of a blood pressure cuff around one thigh served as a stimulus for testing dynamic autoregulation. Both measurements were performed in patients with intact autoregulation during propofol anesthesia and again in the same patients after autoregulation had been impaired by administration of high-dose isoflurane. There was a significant reduction in autoregulatory capacity after the administration of high-dose isoflurane, which could be demonstrated using static (P < .0001) and dynamic (P < .0001) methods. The correlation between static or steady-state and dynamic autoregulation measurements was highly significant (r = .93, P < .0001). These data show that in normal human subjects measurement of dynamic autoregulation yields similar results as static testing of intact and pharmacologically impaired autoregulation.

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Cerebral blood flow during exercise: mechanisms of regulation.

Shigehiko Ogoh, Philip Ainslie (2009)

The response of cerebral vasculature to exercise is different from other peripheral vasculature; it has a small vascular bed and is strongly regulated by cerebral autoregulation and the partial pressure of arterial carbon dioxide (Pa(CO(2))). In contrast to other organs, the traditional thinking is that total cerebral blood flow (CBF) remains relatively constant and is largely unaffected by a variety of conditions, including those imposed during exercise. Recent research, however, indicates that cerebral neuronal activity and metabolism drive an increase in CBF during exercise. Increases in exercise intensity up to approximately 60% of maximal oxygen uptake produce elevations in CBF, after which CBF decreases toward baseline values because of lower Pa(CO(2)) via hyperventilation-induced cerebral vasoconstriction. This finding indicates that, during heavy exercise, CBF decreases despite the cerebral metabolic demand. In contrast, this reduced CBF during heavy exercise lowers cerebral oxygenation and therefore may act as an independent influence on central fatigue. In this review, we highlight methodological considerations relevant for the assessment of CBF and then summarize the integrative mechanisms underlying the regulation of CBF at rest and during exercise. In addition, we examine how CBF regulation during exercise is altered by exercise training, hypoxia, and aging and suggest avenues for future research.

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Pathophysiology of the neurovascular unit: disease cause or consequence?

B Stanimirovic, Alon Friedman (2012)

Pathophysiology of the neurovascular unit (NVU) is commonly seen in neurological diseases. The typical features of NVU pathophysiology include tissue hypoxia, inflammatory and angiogenic activation, as well as initiation of complex molecular interactions between cellular (brain endothelial cells, astroctyes, pericytes, inflammatory cells, and neurons) and acellular (basal lamina) components of the NVU, jointly resulting in increased blood-brain barrier permeability, brain edema, neurovascular uncoupling, and neuronal dysfunction and damage. The evidence of important role of the brain vascular compartment in disease pathogenesis has elicited the debate whether the primary vascular events may be a cause of the neurological disease, as opposed to a mere participant recruited by a primary neuronal origin of pathology? Whereas some hereditary and acquired cerebral angiopathies could be considered a primary cause of neurological symptoms of the disease, the epidemiological studies showing a high degree of comorbidity among vascular disease and dementias, including Alzheimer's disease, as well as migraine and epilepsy, suggested that primary vascular pathology may be etiological factor causing neuronal dysfunction or degeneration in these diseases. This review focuses on recent hypotheses and evidence, suggesting that pathophysiology of the NVU may be initiating trigger for neuronal pathology and subsequent neurological manifestations of the disease.

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Author and article information

Contributors

Timothy W. Secomb: Role: Editor

Journal

Journal ID (nlm-ta): PLoS One

Journal ID (iso-abbrev): PLoS ONE

Journal ID (publisher-id): plos

Journal ID (pmc): plosone

Title: PLoS ONE

Publisher: Public Library of Science (San Francisco, USA )

ISSN (Electronic): 1932-6203

Publication date Collection: 2013

Publication date (Electronic): 14 August 2013

Volume: 8

Issue: 8

Electronic Location Identifier: e70821

Affiliations

[1 ]Department of Neurology, Hospital das Clinicas, University of São Paulo School of Medicine, São Paulo, Brazil

[2 ]Department of Neurosurgery, Hospital das Clinicas, University of São Paulo School of Medicine, São Paulo, Brazil

[3 ]Heart Institute (InCor), University of São Paulo Medical School, São Paulo; School of Physical Education and Sport, University of São Paulo, São Paulo, Brazil

[4 ]Medical Physics Group, Department of Cardiovascular Sciences, University of Leicester, Leicester Royal Infirmary, Leicester, England

[5 ]Biomedical Research Unit in Cardiovascular Science, Glenfield Hospital, Leicester, England

University of Arizona, United States of America

Author notes

* E-mail: rp9@ 123456le.ac.uk

Competing Interests: The authors have declared that no competing interests exist.

Conceived and designed the experiments: RCN EBSS CEN MJT. Performed the experiments: RCN MRS CEN. Analyzed the data: RCN RBP. Wrote the paper: RCN RBP. Read and approved the final version of the manuscript: RCN EBSS CEN MRS MJT RBP.

Article

Publisher ID: PONE-D-13-09515

DOI: 10.1371/journal.pone.0070821

PMC ID: 3743835

PubMed ID: 23967113

SO-VID: 6ce80a1f-cb67-4423-963b-d0ac49185838

License:

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

History

Date received : 6 March 2013

Date accepted : 23 June 2013

Page count

Pages: 8

Funding

RC Nogueira was supported by a travelling scholarship from CAPES/Brazilian Ministry of Education. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Dynamic Cerebral Autoregulation Changes during Sub-Maximal Handgrip Maneuver

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Abstract

Purpose

Methods

Results

Conclusion

Related collections

PLOS Climate

Most cited references 30

Comparison of static and dynamic cerebral autoregulation measurements.

Cerebral blood flow during exercise: mechanisms of regulation.

Pathophysiology of the neurovascular unit: disease cause or consequence?

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