Matthew R Sanborn1, Mark E Edsell2, Meeri N Kim3, Rickson Mesquita3, Mary E Putt4, Chris Imray5, Heng Yow6, Mark H Wilson6, Arjun G Yodh3, Mike Grocott6, Daniel S Martin6. 1. UCL Centre for Altitude, Space and Extreme Environment Medicine, Portex Unit, Institute of Child Health (Drs Sanborn, Edsell, Imray, Yow, Wilson, Grocott, and Martin), and; Maine Medical Center, Portland, ME (Dr Sanborn). Electronic address: matthewrsanborn@gmail.com. 2. UCL Centre for Altitude, Space and Extreme Environment Medicine, Portex Unit, Institute of Child Health (Drs Sanborn, Edsell, Imray, Yow, Wilson, Grocott, and Martin), and; St. George's Hospital (Dr Edsell), London, UK. 3. Departments of Physics and Astronomy (Drs Kim, Mesquita, and Yodh). 4. Biostatistics and Epidemiology (Dr Putt), University of Pennsylvania, Philadelphia, PA. 5. UCL Centre for Altitude, Space and Extreme Environment Medicine, Portex Unit, Institute of Child Health (Drs Sanborn, Edsell, Imray, Yow, Wilson, Grocott, and Martin), and; University Hospitals Coventry and Warwickshire NHS Trust, Warwick Medical School, Coventry, UK (Dr Imray); and. 6. UCL Centre for Altitude, Space and Extreme Environment Medicine, Portex Unit, Institute of Child Health (Drs Sanborn, Edsell, Imray, Yow, Wilson, Grocott, and Martin), and.
Abstract
OBJECTIVE: Alterations in cerebral blood flow (CBF) and cerebral oxygenation are implicated in altitude-associated diseases. We assessed the dynamic changes in CBF and peripheral and cerebral oxygenation engendered by ascent to altitude with partial acclimatization and hyperventilation using a combination of near-infrared spectroscopy, transcranial Doppler ultrasound, and diffuse correlation spectroscopy. METHODS: Peripheral (Spo2) and cerebral (Scto2) oxygenation, end-tidal carbon dioxide (ETCO2), and cerebral hemodynamics were studied in 12 subjects using transcranial Doppler and diffuse correlation spectroscopy (DCS) at 75 m and then 2 days and 7 days after ascending to 4559 m above sea level. After obtaining baseline measurements, subjects hyperventilated to reduce baseline ETCO2 by 50%, and a further set of measurements were obtained. RESULTS: Cerebral oxygenation and peripheral oxygenation showed a divergent response, with cerebral oxygenation decreasing at day 2 and decreasing further at day 7 at altitude, whereas peripheral oxygenation decreased on day 2 before partially rebounding on day 7. Cerebral oxygenation decreased after hyperventilation at sea level (Scto2 from 68.8% to 63.5%; P<.001), increased after hyperventilation after 2 days at altitude (Scto2 from 65.6% to 69.9%; P=.001), and did not change after hyperventilation after 7 days at altitude (Scto2 from 62.2% to 63.3%; P=.35). CONCLUSIONS: An intensification of the normal cerebral hypocapnic vasoconstrictive response occurred after partial acclimatization in the setting of divergent peripheral and cerebral oxygenation. This may help explain why hyperventilation fails to improve cerebral oxygenation after partial acclimatization as it does after initial ascent. The use of DCS is feasible at altitude and provides a direct measure of CBF indices with high temporal resolution.
OBJECTIVE: Alterations in cerebral blood flow (CBF) and cerebral oxygenation are implicated in altitude-associated diseases. We assessed the dynamic changes in CBF and peripheral and cerebral oxygenation engendered by ascent to altitude with partial acclimatization and hyperventilation using a combination of near-infrared spectroscopy, transcranial Doppler ultrasound, and diffuse correlation spectroscopy. METHODS: Peripheral (Spo2) and cerebral (Scto2) oxygenation, end-tidal carbon dioxide (ETCO2), and cerebral hemodynamics were studied in 12 subjects using transcranial Doppler and diffuse correlation spectroscopy (DCS) at 75 m and then 2 days and 7 days after ascending to 4559 m above sea level. After obtaining baseline measurements, subjects hyperventilated to reduce baseline ETCO2 by 50%, and a further set of measurements were obtained. RESULTS: Cerebral oxygenation and peripheral oxygenation showed a divergent response, with cerebral oxygenation decreasing at day 2 and decreasing further at day 7 at altitude, whereas peripheral oxygenation decreased on day 2 before partially rebounding on day 7. Cerebral oxygenation decreased after hyperventilation at sea level (Scto2 from 68.8% to 63.5%; P<.001), increased after hyperventilation after 2 days at altitude (Scto2 from 65.6% to 69.9%; P=.001), and did not change after hyperventilation after 7 days at altitude (Scto2 from 62.2% to 63.3%; P=.35). CONCLUSIONS: An intensification of the normal cerebral hypocapnic vasoconstrictive response occurred after partial acclimatization in the setting of divergent peripheral and cerebral oxygenation. This may help explain why hyperventilation fails to improve cerebral oxygenation after partial acclimatization as it does after initial ascent. The use of DCS is feasible at altitude and provides a direct measure of CBF indices with high temporal resolution.
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