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@INPROCEEDINGS{Michno:1027709,
author = {Michno, M. and Weis, H. and Schmitz, J. and Foerges, Anna
Linea and Beer, Simone and Neumaier, B. and Drzezga, A. and
Aeschbach, D. and Bauer, Andreas and Tank, J. and
Elmenhorst, E. and Elmenhorst, D.},
title = {{E}ffect of acute hypoxia exposure on the availability of
{A}1 adenosine receptors in the human brain measured with
[{F}-18]{CPFPX} {PET}},
reportid = {FZJ-2024-04019},
year = {2023},
abstract = {Ziel/Aim Normobaric hypoxia induces numerous adaptive
changes, e. g., incerebral blood flow, metabolism and
electrical activity. Adenosine, as an
inhibitoryneuromodulator, is produced in and/or released to
the interstitial spaceduring hypoxia and assumed to mediate
several of these effects. A1 adenosinereceptor (A1AR)
antagonism or knock-out attenuates this neuronal
inhibitionin mice. Here we tested the hypothesis that
exposure to an interval of hypoxiacompared to an interval of
normoxia (control) reduces the availability of A1ARin the
human brain, due to hypoxia-triggered rise of endogenous
adenosine.As exploratory objectives, we tested the
hypotheses that psychomotor vigilanceis affected during
hypoxia and that cerebral blood flow is
altered.Methodik/Methods Ten healthy volunteers (32 ± 13
years, 3f) completed an110-min bolus plus constant infusion
[F-18]CPFPX PET-MRI hybrid experiment:Subjects spent the
first 60 minutes of the scan in normoxia followed by
30minutes of individually adapted normobaric hypoxia to
achieve a peripheraloxygen saturation of 70 - 75 $\%,$
followed by 20 minutes of normoxia. Bloodsamples were used
to calculate metabolite-corrected steady-state
distributionvolumes (VT) of A1AR (i. e., 40 – 100 min
after start of [F-18]CPFPX administration).Brain perfusion
was measured via arterial spin labelling. A
3-minutepsychomotor vigilance test (PVT) was conducted every
10 minutes. Heart rateand peripheral blood oxygen saturation
were measured continuously.Ergebnisse/Results Hypoxia
reduced A1AR availability in the cerebral cortexby 11 $\%$
(p = 0.033). Compared to normoxia, brain perfusion increased
duringhypoxia by 25 $\%$ in cortical gray matter (p <
0.001). Heart rate increased by 22 $\%(p$ < 0.001). PVT mean
reaction time was longer by 7 ms (p =
0.027).Schlussfolgerungen/Conclusions Short term reduction
of the oxygen saturationto 70 $\%$ (corresponding to an
oxygen saturation at an altitude of approximately6000 m)
increases cerebral blood flow and impairs cognitive
performancewhile A1AR availability is reduced. This
indicates that acute hypoxiaexposure increases cerebral
adenosine concentration and receptor occupancy.},
month = {Apr},
date = {2023-04-19},
organization = {61. Jahrestagung der Deutschen
Gesellschaft für Nuklearmedizin,
Leipzig (Germany), 19 Apr 2023 - 22 Apr
2023},
subtyp = {After Call},
cin = {INM-5},
cid = {I:(DE-Juel1)INM-5-20090406},
pnm = {5253 - Neuroimaging (POF4-525)},
pid = {G:(DE-HGF)POF4-5253},
typ = {PUB:(DE-HGF)6},
doi = {10.1055/s-0043-1766157},
url = {https://juser.fz-juelich.de/record/1027709},
}