scholarly journals Central respiratory chemosensitivity and cerebrovascular CO2 reactivity: a rebreathing demonstration illustrating integrative human physiology

2016 ◽  
Vol 40 (1) ◽  
pp. 79-92 ◽  
Author(s):  
Christina M. MacKay ◽  
Rachel J. Skow ◽  
Michael M. Tymko ◽  
Lindsey M. Boulet ◽  
Margie H. Davenport ◽  
...  

One of the most effective ways of engaging students of physiology and medicine is through laboratory demonstrations and case studies that combine 1) the use of equipment, 2) problem solving, 3) visual representations, and 4) manipulation and interpretation of data. Depending on the measurements made and the type of test, laboratory demonstrations have the added benefit of being able to show multiple organ system integration. Many research techniques can also serve as effective demonstrations of integrative human physiology. The “Duffin” hyperoxic rebreathing test is often used in research settings as a test of central respiratory chemosensitivity and cerebrovascular reactivity to CO2. We aimed to demonstrate the utility of the hyperoxic rebreathing test for both respiratory and cerebrovascular responses to increases in CO2 and illustrate the integration of the respiratory and cerebrovascular systems. In the present article, methods such as spirometry, respiratory gas analysis, and transcranial Doppler ultrasound are described, and raw data traces can be adopted for discussion in a tutorial setting. If educators have these instruments available, instructions on how to carry out the test are provided so students can collect their own data. In either case, data analysis and quantification are discussed, including principles of linear regression, calculation of slope, the coefficient of determination ( R2), and differences between plotting absolute versus normalized data. Using the hyperoxic rebreathing test as a demonstration of the complex interaction and integration between the respiratory and cerebrovascular systems provides senior undergraduate, graduate, and medical students with an advanced understanding of the integrative nature of human physiology.

2012 ◽  
Vol 124 (3) ◽  
pp. 177-189 ◽  
Author(s):  
Damian M. Bailey ◽  
Daniel W. Jones ◽  
Andrew Sinnott ◽  
Julien V. Brugniaux ◽  
Karl J. New ◽  
...  

The present study examined to what extent professional boxing compromises cerebral haemodynamic function and its association with CTBI (chronic traumatic brain injury). A total of 12 male professional boxers were compared with 12 age-, gender- and physical fitness-matched non-boxing controls. We assessed dCA (dynamic cerebral autoregulation; thigh-cuff technique and transfer function analysis), CVRCO2 (cerebrovascular reactivity to changes in CO2: 5% CO2 and controlled hyperventilation), orthostatic tolerance (supine to standing) and neurocognitive function (psychometric tests). Blood flow velocity in the middle cerebral artery (transcranial Doppler ultrasound), mean arterial blood pressure (finger photoplethysmography), end-tidal CO2 (capnography) and cortical oxyhaemoglobin concentration (near-IR spectroscopy) were continuously measured. Boxers were characterized by fronto-temporal neurocognitive dysfunction and impaired dCA as indicated by a lower rate of regulation and autoregulatory index (P<0.05 compared with controls). Likewise, CVRCO2 was also reduced resulting in a lower CVRCO2 range (P<0.05 compared with controls). The latter was most marked in boxers with the highest CTBI scores and correlated against the volume and intensity of sparring during training (r=−0.84, P<0.05). These impairments coincided with more marked orthostatic hypotension, cerebral hypoperfusion and corresponding cortical de-oxygenation during orthostatic stress (P<0.05 compared with controls). In conclusion, these findings provide the first comprehensive evidence for chronically impaired cerebral haemodynamic function in active boxers due to the mechanical trauma incurred by repetitive, sub-concussive head impact incurred during sparring training. This may help explain why CTBI is a progressive disease that manifests beyond the active boxing career.


2008 ◽  
Vol 12 (1) ◽  
pp. 11-15
Author(s):  
George Kwok-Chu Wong ◽  
Stephanie Chi-Ping Ng ◽  
Matthew Tak-Vai Chan ◽  
David Tin-Fung Sun ◽  
Wynnie Wai-Man Lam ◽  
...  

PeerJ ◽  
2013 ◽  
Vol 1 ◽  
pp. e65 ◽  
Author(s):  
Michelle N. McDonnell ◽  
Narelle M. Berry ◽  
Mark A. Cutting ◽  
Hannah A. Keage ◽  
Jonathan D. Buckley ◽  
...  

1993 ◽  
Vol 264 (6) ◽  
pp. H2124-H2130
Author(s):  
P. J. St Jacques ◽  
J. R. Kirsch ◽  
M. N. Diringer ◽  
R. J. Traystman

We tested the hypothesis that severe insulin-induced hypoglycemia would depress cerebrovascular reactivity to CO2 via a mechanism that could be prevented by administration of the N-methyl-D-aspartate (NMDA) receptor antagonist MK-801 in infant piglets. Cerebral blood flow (CBF) was measured (microspheres) in 2- to 3-wk-old pentobarbital-anesthetized piglets during hypocapnia, normocapnia, and hypercapnia. Repeat CBF measurements were made either 1 (n = 5) or 2 h (n = 6) after insulin (200 U/kg iv) to elicit the time course of altered reactivity to CO2. Repeat CBF measurements were made in a third group (n = 5) 2 h after treatment with insulin and MK-801 (1.5 mg/kg iv bolus, 0.15 mg.kg-1.h-1 iv infusion) to determine whether any alteration in reactivity to CO2 was due to a mechanism involving the NMDA receptor. Cerebrovascular resistance and cerebral O2 consumption (CMRO2) were calculated with each measurement of CBF. Cerebrovascular response to CO2 (change in cerebrovascular resistance/change in arterial CO2 tension) was ablated in the group of piglets exposed to 1 or 2 h of hypoglycemia (preinsulin 1-h group, 0.038 +/- 0.007; preinsulin 2-h group, 0.023 +/- 0.004 mmHg.ml-1.min.100 g.mmHg CO2(-1)). Treatment with MK-801 did not alter normoglycemic CO2 reactivity (preinsulin, 0.032 +/- 0.005 mmHg.ml-1.min.100 g.mmHg CO2(-1)) and did not prevent ablation of cerebrovascular CO2 reactivity during hypoglycemia. CMRO2 was not affected by hypoglycemia in any group.(ABSTRACT TRUNCATED AT 250 WORDS)


Author(s):  
Andrew G. Pearson ◽  
Kathleen B. Miller ◽  
Adam T. Corkery ◽  
Nicole A. Eisenmann ◽  
Anna J. Howery ◽  
...  

Structural and functional changes in the cerebral vasculature occur with advancing age, which may lead to impaired neurovascular coupling (NVC) and cognitive decline. Cyclooxygenase (COX) inhibition abolishes age-related differences in cerebrovascular reactivity, but it is unclear if COX inhibition impacts NVC. The purpose of this study was to examine the influence of aging on NVC before and after COX inhibition. Twenty-three young (age=25±4 y) and 21 older (age=64±5 y) adults completed two levels of difficulty of the Stroop and n-back tests before and after COX inhibition. Middle cerebral artery blood velocity (MCAv) was measured using transcranial Doppler ultrasound and mean arterial blood pressure (MAP) was measured using a finger cuff. Hemodynamic variables were measured at rest and in response to cognitive challenges. During the Stroop test, older adults demonstrated a greater increase in MCAv (Young: 2.2±6.8% vs. Older: 5.9±5.8%; P=0.030) and MAP (Young: 2.0±4.9% vs. Older: 4.8±4.9%; P=0.036) compared with young adults. There were no age-related differences during the n-back test. COX inhibition reduced MCAv by 30% in young and 26% in older adults (P<0.001 for both). During COX inhibition, there were no age-related differences in the percent change in MCAv or MAP in response to the cognitive tests. Our results show that older adults require greater increases in MCAv and MAP during a test of executive function compared with young adults and that any age-related differences in NVC were abolished during COX inhibition. Collectively, this suggests that aging is associated with greater NVC necessary to accomplish a cognitive task.


2014 ◽  
Vol 49 (16) ◽  
pp. 1050-1055 ◽  
Author(s):  
Andrew J Gardner ◽  
Can Ozan Tan ◽  
Philip N Ainslie ◽  
Paul van Donkelaar ◽  
Peter Stanwell ◽  
...  

2017 ◽  
Vol 129 ◽  
pp. 61S-62S
Author(s):  
Montoya Eliana ◽  
Jorge Carrizosa ◽  
Alejandro Castro ◽  
Alexander Sanchez ◽  
Reinaldo Nino

2009 ◽  
Vol 296 (5) ◽  
pp. R1473-R1495 ◽  
Author(s):  
Philip N. Ainslie ◽  
James Duffin

Cerebral blood flow (CBF) and its distribution are highly sensitive to changes in the partial pressure of arterial CO2 (PaCO2). This physiological response, termed cerebrovascular CO2 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 CO2 from brain tissue, thereby attenuating the rise in central Pco2, whereas hypocapnia causes cerebral vasoconstriction, which reduces CBF and attenuates the fall of brain tissue Pco2. Cerebrovascular reactivity and ventilatory response to PaCO2 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 CO2, 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 CO2 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 PaCO2, that control CBF. We discuss in detail the assessment and interpretation of cerebrovascular reactivity to CO2. Next, we provide a detailed update on the integration of the role of cerebrovascular CO2 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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