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of Victoria
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Faculty of Graduate Studies

Destiny Underwood

  • BSc (Camosun College, 2022)

Notice of the Final Oral Examination for the Degree of Master of Science

Topic

Mechanisms of cerebral artery compliance at sea-level and following acclimation to high altitude

School of Exercise Science, Physical and Health Education

Date & location

  • Wednesday, March 24, 2024

  • 11:30 A.M.

  • McKinnon Building

  • Room 155

Reviewers

Supervisory Committee

  • Dr. Kurt Smith, School of Exercise Science, Physical & Health Education, University of Victoria (Supervisor)

  • Dr. David Kennedy, School of Exercise Science, Physical & Health Education, UVic (Member) 

External Examiner

  • Dr. Ryan Hoiland, Department of Medical Science, University of British Columbia 

Chair of Oral Examination

  • Dr. Neil Ernst, Department of Computer Science, UVic

     

Abstract

Brain health is dependent on adequate cerebral blood flow (CBF) delivered through healthy compliant vessels that buffer pulsatile hemodynamic stress. Pharmacological interventions at sea-level (SL) and high altitude (HA, 5050m) that increase and lower CBF provide a useful experimental design to assess the mechanisms involved in buffering cerebrovascular hemodynamic stress. We characterized pulsatile hemodynamic damping factors (DFi), as an index of cerebral hemodynamic stress. DFi was calculated from pulsitility (PI) in the internal carotid (ICA) and middle cerebral arteries (MCA) at SL and HA following pharmacological attempts to increase (SL=Dobutamine, DOB; HA = DOB+Actetazolamide, DOB+ACZ) and decrease (Indomethacin; INDO) CBF in healthy lowlander adults (n=12, 4 females). Cerebrovascular hemodynamics in the ICA (flow [QICA], PIICA) and MCA (velocity [MCAv], PIMCA) were measured using ultrasound; DFi=PIICA:PIMCA. Administration of DOB (2 (5μg/kg/min) at SL, DOB+ACZ (5μg/kg/min+10 mg/kg) at HA, and INDO (1.45 mg/kg) at SL and HA were performed on separate days in randomized order. No QICA response were observed following DOB, while QICA increased following DOB+ACZ (D+41 cm.s-1, p=0.01), and decreased following INDO at SL (D-53 cm.s-1,p=0.04) and HA (D-41 cm.s-1, p=0.004). DOB and DOB+ACZ administration differentially altered HR (D-3 bpm;D+5 bpm, p=0.02), DICAV (D-6 cm.s-1; D+10 cm.s-1; p=0.04), MCAv (D+0 cm.s-1; D+17 cm.s-1), and PIICA (D+0.4 a.u; D+0.2 a.u.; p=0.03). DOB reduced DFi (D-0.1, p=0.02). Meanwhile DFi following INDO was significantly lower at HA (D-0.54 a.u, p=0.02) but not at SL (D-0.26 a.u, p=0.18). The results from these two field experiments highlights that reducing CBF via cyclooxygenase inhibition detrimental alters the buffering of cerebrovascular hemodynamic stress. In contrast, at HA when CBF is increased following DOB+ACZ cerebrovascular hemodynamic regulation was preserved.

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