by Magdalena Wszedybyl-Winklewska, Jacek Wolf, Ewa Swierblewska, Katarzyna Kunicka, Agnieszka Gruszecka, Marcin Gruszecki, Wieslawa Kucharska, Pawel J. Winklewski, Joanna Zabulewicz, Wojciech Guminski, Michal Pietrewicz, Andrzej F. Frydrychowski, Leszek Bieniaszewski, Krzysztof Narkiewicz
BackgroundAcute hypoxia exerts strong effects on the cardiovascular system. Heart-generated pulsatile cerebrospinal fluid motion is recognised as a key factor ensuring brain homeostasis. We aimed to assess changes in heart-generated coupling between blood pressure (BP) and subarachnoid space width (SAS) oscillations during hypoxic exposure.
MethodsTwenty participants were subjected to a controlled decrease in oxygen saturation (SaO2 = 80%) for five minutes. BP and heart rate (HR) were measured using continuous finger-pulse photoplethysmography, oxyhaemoglobin saturation with an ear-clip sensor, end-tidal CO2 with a gas analyser, and cerebral blood flow velocity (CBFV), pulsatility and resistive indices with Doppler ultrasound. Changes in SAS were recorded with a recently-developed method called near-infrared transillumination/backscattering sounding. Wavelet transform analysis was used to assess the relationship between BP and SAS oscillations.
ResultsGradual increases in systolic, diastolic BP and HR were observed immediately after the initiation of hypoxic challenge (at fifth minute +20.1%, +10.2%, +16.5% vs. baseline, respectively; all P Conclusions
Cerebral haemodynamics seem to be relatively stable during short exposure to normobaric hypoxia. Hypoxia attenuates heart-generated BP SAS coupling.
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