001027709 001__ 1027709
001027709 005__ 20250203103452.0
001027709 0247_ $$2doi$$a10.1055/s-0043-1766157
001027709 037__ $$aFZJ-2024-04019
001027709 1001_ $$0P:(DE-Juel1)191151$$aMichno, M.$$b0$$eCorresponding author$$ufzj
001027709 1112_ $$a61. Jahrestagung der Deutschen Gesellschaft für Nuklearmedizin$$cLeipzig$$d2023-04-19 - 2023-04-22$$wGermany
001027709 245__ $$aEffect of acute hypoxia exposure on the availability of A1 adenosine receptors in the human brain measured with [F-18]CPFPX PET
001027709 260__ $$c2023
001027709 3367_ $$033$$2EndNote$$aConference Paper
001027709 3367_ $$2DataCite$$aOther
001027709 3367_ $$2BibTeX$$aINPROCEEDINGS
001027709 3367_ $$2DRIVER$$aconferenceObject
001027709 3367_ $$2ORCID$$aLECTURE_SPEECH
001027709 3367_ $$0PUB:(DE-HGF)6$$2PUB:(DE-HGF)$$aConference Presentation$$bconf$$mconf$$s1719375542_17792$$xAfter Call
001027709 520__ $$aZiel/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.
001027709 536__ $$0G:(DE-HGF)POF4-5253$$a5253 - Neuroimaging (POF4-525)$$cPOF4-525$$fPOF IV$$x0
001027709 588__ $$aDataset connected to CrossRef Conference
001027709 7001_ $$0P:(DE-HGF)0$$aWeis, H.$$b1
001027709 7001_ $$0P:(DE-HGF)0$$aSchmitz, J.$$b2
001027709 7001_ $$0P:(DE-Juel1)179271$$aFoerges, Anna Linea$$b3$$ufzj
001027709 7001_ $$0P:(DE-Juel1)133864$$aBeer, Simone$$b4$$ufzj
001027709 7001_ $$0P:(DE-Juel1)166419$$aNeumaier, B.$$b5$$ufzj
001027709 7001_ $$0P:(DE-Juel1)177611$$aDrzezga, A.$$b6$$ufzj
001027709 7001_ $$0P:(DE-HGF)0$$aAeschbach, D.$$b7
001027709 7001_ $$0P:(DE-Juel1)131672$$aBauer, Andreas$$b8$$ufzj
001027709 7001_ $$0P:(DE-HGF)0$$aTank, J.$$b9
001027709 7001_ $$0P:(DE-HGF)0$$aElmenhorst, E.$$b10
001027709 7001_ $$0P:(DE-Juel1)131679$$aElmenhorst, D.$$b11$$ufzj
001027709 773__ $$a10.1055/s-0043-1766157
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001027709 9101_ $$0I:(DE-588b)5008462-8$$6P:(DE-Juel1)191151$$aForschungszentrum Jülich$$b0$$kFZJ
001027709 9101_ $$0I:(DE-588b)5008462-8$$6P:(DE-Juel1)179271$$aForschungszentrum Jülich$$b3$$kFZJ
001027709 9101_ $$0I:(DE-588b)5008462-8$$6P:(DE-Juel1)133864$$aForschungszentrum Jülich$$b4$$kFZJ
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001027709 9101_ $$0I:(DE-588b)5008462-8$$6P:(DE-Juel1)177611$$aForschungszentrum Jülich$$b6$$kFZJ
001027709 9101_ $$0I:(DE-588b)5008462-8$$6P:(DE-Juel1)131672$$aForschungszentrum Jülich$$b8$$kFZJ
001027709 9101_ $$0I:(DE-588b)5008462-8$$6P:(DE-Juel1)131679$$aForschungszentrum Jülich$$b11$$kFZJ
001027709 9131_ $$0G:(DE-HGF)POF4-525$$1G:(DE-HGF)POF4-520$$2G:(DE-HGF)POF4-500$$3G:(DE-HGF)POF4$$4G:(DE-HGF)POF$$9G:(DE-HGF)POF4-5253$$aDE-HGF$$bKey Technologies$$lNatural, Artificial and Cognitive Information Processing$$vDecoding Brain Organization and Dysfunction$$x0
001027709 9141_ $$y2024
001027709 920__ $$lyes
001027709 9201_ $$0I:(DE-Juel1)INM-5-20090406$$kINM-5$$lNuklearchemie$$x0
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001027709 980__ $$aI:(DE-Juel1)INM-5-20090406
001027709 980__ $$aUNRESTRICTED