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Your search keyword '"Rieger, Mathew G."' showing total 9 results
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9 results on '"Rieger, Mathew G."'

2. The influence of sex and maturation on carotid and vertebral artery hemodynamics and associations with free-living (in)activity in 6-17 year-olds

Author

Tallon, Christine M., primary, Smith, Kurt Jason, additional, Nowak-Flück, Daniela, additional, Koziol, Alyssa V., additional, Rieger, Mathew G., additional, Lutes, Lesley D., additional, Green, Daniel J., additional, Tremblay, Mark S., additional, Ainslie, Philip N., additional, and McManus, Ali Mary, additional

Published
2021
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3. UBC-Nepal Expedition:Haemoconcentration underlies the reductions in cerebral blood flow observed during acclimatization to high altitude

Author

Howe, Connor A, Ainslie, Philip N, Tremblay, Joshua C, Carter, Howard Henry, Patrician, Alex, Stembridge, Mike, Williams, Alex, Drane, Aimee L, Delorme, Eric, Rieger, Mathew G, Tymko, Michael M, Gasho, Chris, Santoro, Antoinette, MacLeod, David B, Hoiland, Ryan L, Howe, Connor A, Ainslie, Philip N, Tremblay, Joshua C, Carter, Howard Henry, Patrician, Alex, Stembridge, Mike, Williams, Alex, Drane, Aimee L, Delorme, Eric, Rieger, Mathew G, Tymko, Michael M, Gasho, Chris, Santoro, Antoinette, MacLeod, David B, and Hoiland, Ryan L

Abstract

At high altitude, an increase in haematocrit (Hct) is achieved through altitude‐induced diuresis and erythropoiesis, both of which result in increased arterial oxygen content. Given the impact of alterations in Hct on oxygen content, haemoconcentration has been hypothesized to mediate, in part, the attenuation of the initial elevation in cerebral blood flow (CBF) at high altitude. To test this hypothesis, healthy men (n = 13) ascended to 5050 m over 9 days without the aid of prophylactic acclimatization medications. After 1 week of acclimatization at 5050 m, participants were haemodiluted by rapid saline infusion (2.10 ± 0.28 l) to return Hct towards pre‐acclimatization values. Arterial blood gases, Hct, global CBF (duplex ultrasound) and haemodynamic variables were measured after initial arrival at 5050 m and after 1 week of acclimatization at high altitude, before and after the haemodilution protocol. After 1 week at 5050 m, the Hct increased from 42.5 ± 2.5 to 49.6 ± 2.5% (P < 0.001), and it was subsequently reduced to 45.6 ± 2.3% (P < 0.001) after haemodilution. Global CBF decreased from 844 ± 160 to 619 ± 136 ml min−1 (P = 0.033) after 1 week of acclimatization and increased to 714 ± 204 ml min−1 (P = 0.045) after haemodilution. Despite the significant changes in Hct, and thus oxygen content, cerebral oxygen delivery was unchanged at all time points. Furthermore, these observations occurred in the absence of any changes in mean arterial blood pressure, cardiac output, arterial blood pH or oxygen saturation pre‐ and posthaemodilution. These data highlight the influence of Hct in the regulation of CBF and are the first to demonstrate experimentally that haemoconcentration contributes to the reduction in CBF during acclimatization to altitude.

Published
2019

4. UBC‐Nepal Expedition: Haemoconcentration underlies the reductions in cerebral blood flow observed during acclimatization to high altitude

Author

Howe, Connor A., primary, Ainslie, Philip N., additional, Tremblay, Joshua C., additional, Carter, Howard H., additional, Patrician, Alex, additional, Stembridge, Mike, additional, Williams, Alex, additional, Drane, Aimee L., additional, Delorme, Eric, additional, Rieger, Mathew G., additional, Tymko, Michael M., additional, Gasho, Chris, additional, Santoro, Antoinette, additional, MacLeod, David B., additional, and Hoiland, Ryan L., additional

Published
2019
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6. Adenosine receptor-dependent signaling is not obligatory for normobaric and hypobaric hypoxia-induced cerebral vasodilation in humans

Author

Hoiland, Ryan L., primary, Bain, Anthony R., additional, Tymko, Michael M., additional, Rieger, Mathew G., additional, Howe, Connor A., additional, Willie, Christopher K., additional, Hansen, Alex B., additional, Flück, Daniela, additional, Wildfong, Kevin W., additional, Stembridge, Mike, additional, Subedi, Prajan, additional, Anholm, James, additional, and Ainslie, Philip N., additional

Published
2017
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9. Hypoxemia, oxygen content, and the regulation of cerebral blood flow.

Author

Hoiland RL, Bain AR, Rieger MG, Bailey DM, and Ainslie PN

Subjects
Acclimatization, Adenosine Triphosphate metabolism, Altitude, Altitude Sickness blood, Altitude Sickness physiopathology, Animals, Cerebral Arteries physiopathology, Hemodilution, Hemoglobins metabolism, Homeostasis, Humans, Hypoxia physiopathology, Nitric Oxide metabolism, Signal Transduction, Cerebral Arteries metabolism, Cerebrovascular Circulation, Hypoxia blood, Oxygen blood, Vasodilation
Abstract

This review highlights the influence of oxygen (O2) availability on cerebral blood flow (CBF). Evidence for reductions in O2 content (CaO2 ) rather than arterial O2 tension (PaO2 ) as the chief regulator of cerebral vasodilation, with deoxyhemoglobin as the primary O2 sensor and upstream response effector, is discussed. We review in vitro and in vivo data to summarize the molecular mechanisms underpinning CBF responses during changes in CaO2 . We surmise that 1) during hypoxemic hypoxia in healthy humans (e.g., conditions of acute and chronic exposure to normobaric and hypobaric hypoxia), elevations in CBF compensate for reductions in CaO2 and thus maintain cerebral O2 delivery; 2) evidence from studies implementing iso- and hypervolumic hemodilution, anemia, and polycythemia indicate that CaO2 has an independent influence on CBF; however, the increase in CBF does not fully compensate for the lower CaO2 during hemodilution, and delivery is reduced; and 3) the mechanisms underpinning CBF regulation during changes in O2 content are multifactorial, involving deoxyhemoglobin-mediated release of nitric oxide metabolites and ATP, deoxyhemoglobin nitrite reductase activity, and the downstream interplay of several vasoactive factors including adenosine and epoxyeicosatrienoic acids. The emerging picture supports the role of deoxyhemoglobin (associated with changes in CaO2 ) as the primary biological regulator of CBF. The mechanisms for vasodilation therefore appear more robust during hypoxemic hypoxia than during changes in CaO2 via hemodilution. Clinical implications (e.g., disorders associated with anemia and polycythemia) and future study directions are considered., (Copyright © 2016 the American Physiological Society.)

Published
2016
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