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| Home > Publications database > Effect of acute hypoxia exposure on the availability of A1 adenosine receptors in the human brain measured with [F-18]CPFPX PET |
| Home > Publications database > Effect of acute hypoxia exposure on the availability of A1 adenosine receptors in the human brain measured with [F-18]CPFPX PET |
| Conference Presentation (After Call) | FZJ-2024-04019 |
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2023
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Please use a persistent id in citations: doi:10.1055/s-0043-1766157
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.
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