Mechanisms of cerebral artery compliance at sea-level and following acclimatization to high altitude.
| dc.contributor.author | Underwood, Destiny | |
| dc.contributor.supervisor | Smith, Kurt | |
| dc.date.accessioned | 2024-04-09T17:25:02Z | |
| dc.date.available | 2024-04-09T17:25:02Z | |
| dc.date.issued | 2024 | |
| dc.degree.department | School of Exercise Science, Physical and Health Education | |
| dc.degree.level | Master of Science MSc | |
| dc.description.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 (change+41±24 ml.min-1, p=0.01), and decreased following INDO at SL (change-53± 56 ml.min-1,p=0.04) and HA (change -41± 18 ml.min-1, p=0.004). DOB and DOB+ACZ administration differentially altered HR (change-3 bpm; change+5 bpm, p=0.02), ICAV (change-6 ± 10 cm.s-1; change+10 ± 11 cm.s-1; p=0.04), MCAv (change+0 ± 10 cm.s-1; change+17± 5 cm.s-1), and PIICA (change+0.4 ± 0.2 a.u; change +0.2 ± 0.09 a.u.; p=0.03). DOB reduced DFi (change -0.1± 0.05, p=0.02) at SL. Meanwhile DFi following INDO was significantly lower at HA (change -0.54± 0.3a.u, p=0.02) but not at SL (change -0.26± 0.3 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 forces. In contrast, at HA when CBF is increased following DOB+ACZ cerebrovascular hemodynamic regulation was preserved. | |
| dc.description.scholarlevel | Graduate | |
| dc.identifier.bibliographicCitation | Mechanisms of cerebral artery compliance at sea-level and following acclimation to high altitude. Underwood Destiny R1, Craig Tabitha V1, Smith, Brianne D1, Day Trevor2, Willie Chris K3, Lucas Samuel JE4, Burgess Keith R. 5,6, Ainslie Philip N2, Smith Kurt J1. I was responsible for all data analysis and interpretation, written presentation of results, and the conceptualization of the secondary analysis and manuscript preparation for submission to the Journal of Experimental Physiology in 2024. | |
| dc.identifier.uri | https://hdl.handle.net/1828/16356 | |
| dc.language | English | eng |
| dc.language.iso | en | |
| dc.rights | Available to the World Wide Web | |
| dc.subject | Cerebral blood flow | |
| dc.subject | High altitude | |
| dc.subject | Transcranial doppler | |
| dc.subject | Ultrasound | |
| dc.subject | Vascular Duplex Ultrasound | |
| dc.subject | Damping factor | |
| dc.title | Mechanisms of cerebral artery compliance at sea-level and following acclimatization to high altitude. | |
| dc.type | Thesis |