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000274066 037__ $$aDZNE-2025-00047
000274066 041__ $$aEnglish
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000274066 1001_ $$aMichno, Manuel$$b0
000274066 245__ $$aEffect of Acute Hypoxia Exposure on the Availability of A1 Adenosine Receptors and Perfusion in the Human Brain.
000274066 260__ $$aNew York, NY$$bSoc.$$c2025
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000274066 520__ $$aIn animal studies it has been observed that the inhibitory neuromodulator adenosine is released into the cerebral interstitial space during hypoxic challenges. Adenosine's actions on the A1 adenosine receptor (A1AR) protect the brain from oxygen deprivation and overexertion through adjustments in cerebral blood flow, metabolism, and electric activity. Methods: Using 8-cyclopentyl-3-(3-[18F]fluoropropyl)-1-propylxanthine ([18F]CPFPX), a PET tracer for the A1AR, we tested the hypothesis that hypoxia-induced adenosine release reduces A1AR availability in the human brain. Furthermore, we investigated whether this response is associated with altered brain perfusion and psychomotor vigilance. Ten healthy volunteers completed a 110-min bolus-plus-constant-infusion [18F]CPFPX PET/MRI hybrid experiment including a 30-min interval of normobaric hypoxia with peripheral oxygen saturation between 70% and 75%. We obtained blood samples to calculate metabolite-corrected steady-state A1AR distribution volumes and measured gray matter brain perfusion via arterial spin labeling in high temporal resolution. A 3-min psychomotor vigilance test was conducted every 10 min, and heart rate and peripheral blood oxygen saturation were continuously measured. Results: In all 7 examined brain regions, hypoxia reduced A1AR availability significantly (e.g., frontal lobe, 13.5%; P = 0.0144) whereas gray matter brain perfusion increased (e.g., frontal lobe, 42.5%; P = 0.0007). Heart rate increased by 19% (P = 0.0039). Mean reaction speed decreased by 4.3% (P = 0.0021). Conclusion: Our study is the first, to our knowledge, to demonstrate that acute hypoxia, corresponding to a mean altitude of 5,500 m (18,000 ft), reduces A1AR availability in the human brain. The finding is consistent with hypoxia-induced cerebral adenosine release leading to increased A1AR occupancy.
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000274066 650_7 $$2Other$$aA1AR
000274066 650_7 $$2Other$$aASL
000274066 650_7 $$2Other$$aPET
000274066 650_7 $$2Other$$a[18F]CPFPX
000274066 650_7 $$2Other$$aadenosine receptors
000274066 650_7 $$2Other$$ahypoxia
000274066 650_7 $$2NLM Chemicals$$aReceptor, Adenosine A1
000274066 650_7 $$2NLM Chemicals$$aXanthines
000274066 650_7 $$2NLM Chemicals$$a8-cyclopenta-3-(3-fluoropropyl)-1-propylxanthine
000274066 650_2 $$2MeSH$$aHumans
000274066 650_2 $$2MeSH$$aMale
000274066 650_2 $$2MeSH$$aReceptor, Adenosine A1: metabolism
000274066 650_2 $$2MeSH$$aAdult
000274066 650_2 $$2MeSH$$aBrain: diagnostic imaging
000274066 650_2 $$2MeSH$$aBrain: metabolism
000274066 650_2 $$2MeSH$$aBrain: blood supply
000274066 650_2 $$2MeSH$$aFemale
000274066 650_2 $$2MeSH$$aPositron-Emission Tomography
000274066 650_2 $$2MeSH$$aCerebrovascular Circulation
000274066 650_2 $$2MeSH$$aHypoxia: metabolism
000274066 650_2 $$2MeSH$$aHypoxia: physiopathology
000274066 650_2 $$2MeSH$$aHypoxia: diagnostic imaging
000274066 650_2 $$2MeSH$$aYoung Adult
000274066 650_2 $$2MeSH$$aXanthines
000274066 650_2 $$2MeSH$$aMagnetic Resonance Imaging
000274066 7001_ $$aSchmitz, Jan$$b1
000274066 7001_ $$aFoerges, Anna L$$b2
000274066 7001_ $$aBeer, Simone$$b3
000274066 7001_ $$aJordan, Jens$$b4
000274066 7001_ $$aNeumaier, Bernd$$b5
000274066 7001_ $$0P:(DE-2719)2811239$$aDrzezga, Alexander$$b6$$udzne
000274066 7001_ $$aAeschbach, Daniel$$b7
000274066 7001_ $$aBauer, Andreas$$b8
000274066 7001_ $$aTank, Jens$$b9
000274066 7001_ $$aWeis, Henning$$b10
000274066 7001_ $$aElmenhorst, Eva-Maria$$b11
000274066 7001_ $$aElmenhorst, David$$b12
000274066 773__ $$0PERI:(DE-600)2040222-3$$a10.2967/jnumed.124.268455$$gVol. 66, no. 1, p. 142 - 149$$n1$$p142 - 149$$tJournal of nuclear medicine$$v66$$x0097-9058$$y2025
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