Peaks and valleys: oscillatory cerebral blood flow at high altitude protects cerebral tissue oxygenation.

Autor: Anderson GK; Cerebral and Cardiovascular Physiology Laboratory, Department of Physiology and Anatomy, University of North Texas Health Science Center, Fort Worth, TX, United States of America., Rosenberg AJ; Cerebral and Cardiovascular Physiology Laboratory, Department of Physiology and Anatomy, University of North Texas Health Science Center, Fort Worth, TX, United States of America., Barnes HJ; Cerebral and Cardiovascular Physiology Laboratory, Department of Physiology and Anatomy, University of North Texas Health Science Center, Fort Worth, TX, United States of America., Bird J; Department of Biology, Mount Royal University, Calgary, Alberta, Canada., Pentz B; Department of Biology, Mount Royal University, Calgary, Alberta, Canada., Byman BRM; Department of Biology, Mount Royal University, Calgary, Alberta, Canada., Jendzjowsky N; Institute of Respiratory Medicine & Exercise Physiology, The Lundquist Institute at UCLA Harbor Medical, Torrance, CA, United States of America., Wilson RJA; Hotchkiss Brain Institute and Alberta Children's Hospital Research Institute; Department of Physiology and Pharmacology, University of Calgary, Calgary, Alberta, Canada., Day TA; Department of Biology, Mount Royal University, Calgary, Alberta, Canada., Rickards CA; Cerebral and Cardiovascular Physiology Laboratory, Department of Physiology and Anatomy, University of North Texas Health Science Center, Fort Worth, TX, United States of America.
Jazyk: angličtina
Zdroj: Physiological measurement [Physiol Meas] 2021 Jun 29; Vol. 42 (6). Date of Electronic Publication: 2021 Jun 29.
DOI: 10.1088/1361-6579/ac0593
Abstrakt: Introduction. Oscillatory patterns in arterial pressure and blood flow (at ∼0.1 Hz) may protect tissue oxygenation during conditions of reduced cerebral perfusion and/or hypoxia. We hypothesized that inducing oscillations in arterial pressure and cerebral blood flow at 0.1 Hz would protect cerebral blood flow and cerebral tissue oxygen saturation during exposure to a combination of simulated hemorrhage and sustained hypobaric hypoxia. Methods. Eight healthy human subjects (4 male, 4 female; 30.1 ± 7.6 year) participated in two experiments at high altitude (White Mountain, California, USA; altitude, 3800 m) following rapid ascent and 5-7 d of acclimatization: (1) static lower body negative pressure (LBNP, control condition) was used to induce central hypovolemia by reducing chamber pressure to -60 mmHg for 10 min (0 Hz) , and; (2) oscillatory LBNP where chamber pressure was reduced to -60 mmHg, then oscillated every 5 s between -30 mmHg and -90 mmHg for 10 min (0.1 Hz) . Measurements included arterial pressure, internal carotid artery (ICA) blood flow, middle cerebral artery velocity (MCAv), and cerebral tissue oxygen saturation (ScO 2 ). Results. Forced 0.1 Hz oscillations in mean arterial pressure and mean MCAv were accompanied by a protection of ScO 2 (0.1 Hz: -0.67% ± 1.0%; 0 Hz: -4.07% ± 2.0%; P  = 0.01). However, the 0.1 Hz profile did not protect against reductions in ICA blood flow (0.1 Hz: -32.5% ± 4.5%; 0 Hz: -19.9% ± 8.9%; P  = 0.24) or mean MCAv (0.1 Hz: -18.5% ± 3.4%; 0 Hz: -15.3% ± 5.4%; P  = 0.16). Conclusions. Induced oscillatory arterial pressure and cerebral blood flow led to protection of ScO 2 during combined simulated hemorrhage and sustained hypoxia. This protection was not associated with the preservation of cerebral blood flow suggesting preservation of ScO 2 may be due to mechanisms occurring within the microvasculature.
(© 2021 Institute of Physics and Engineering in Medicine.)
Databáze: MEDLINE
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