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Shahrzad Soleimani Dehnavi
Laval University
Shahrzad Soleimani Dehnavi, a graduate student at Laval University, investigated dynamic cerebral autoregulation (dCA) and its directional sensitivity during mild and severe normobaric hypoxia in 20 participants using oscillatory lower body negative pressure (OLBNP). By analyzing changes in mean arterial pressure (MAP) and cerebral blood flow velocity, the study found that severe hypoxia impaired dCA, reflected by increased variability and reduced buffering capacity of the cerebral circulation, while mild hypoxia had no significant effect. Despite these changes, the hysteresis-like directional sensitivity of dCA remained consistent across all conditions, suggesting it is governed by mechanisms independent of overall autoregulatory capacity. Shahrzad will present this research at the Annual Meeting of the Cerebrovascular Research Network (CARNet), which will take place in September in Liverpool, United Kingdom.
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ABSTRACT
Dynamic cerebral autoregulation (dCA) stabilizes cerebral blood flow (CBF) during rapid mean arterial pressure (MAP) changes and exhibits directional sensitivity, referring to the reduced changes in CBF in response to transient increases compared with decreases in MAP. Hypoxia may impair this regulatory capacity and promote CBF instability. Yet, whether the severity of normobaric poikilocapnic hypoxia differentially influences dCA and its hysteresis-like pattern remains unclear. The aim of this study was to examine the impact of acute mild [fraction of inspired oxygen (FiO₂=0.16)], and severe (FiO₂=0.10) normobaric poikilocapnic hypoxia, compared to normoxia (FiO₂=0.21), on dCA and its directional sensitivity. Twenty participants completed 6-min oscillatory lower body negative pressure (OLBNP) trials at 0.05 and 0.10 Hz in three distinct sessions, where MAP and middle cerebral artery mean blood velocity (MCAv) were continuously recorded. dCA and its hysteresis-like pattern were quantified using transfer function analysis and directional sensitivity analysis for each transition, we calculated relative MCAv and MAP changes with respect to the transition time intervals of both variables indexing time adjusted ratios when MAP increases (%MCAvT/%MAPTINCREASE) and decreases (%MCAvT/%MAPTDECREASE). Acute exposure to severe hypoxia increased MAP (p=0.042) and MCAv (p=0.013) power and decreased TFA phase (p=0.026) only at 0.05 Hz OLBNP compared to normoxia, suggesting impaired dCA. However, mild hypoxia did not influence dCA. Regardless of hypoxia severity, %MCAvT/%MAPTINCREASE was lower than %MCAvT/%MAPTDECREASE at both 0.05 Hz (p=0.007) and 0.10 Hz (p=0.008) OLBNP. These results suggest that acute severe, but not mild normobaric poikilocapnic hypoxia, impairs dCA in the very low frequency range of MAP oscillations, reflecting a reduced buffering capacity of the cerebral circulation. Nonetheless, the hysteresis-like pattern in dCA observed in normoxia is not influenced by mild or severe normobaric poikilocapnic hypoxia, suggesting dCA and its directional sensitivity might be controlled by different autoregulatory mechanisms under this stress.
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