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@ARTICLE{Michno:274066,
author = {Michno, Manuel and Schmitz, Jan and Foerges, Anna L and
Beer, Simone and Jordan, Jens and Neumaier, Bernd and
Drzezga, Alexander and Aeschbach, Daniel and Bauer, Andreas
and Tank, Jens and Weis, Henning and Elmenhorst, Eva-Maria
and Elmenhorst, David},
title = {{E}ffect of {A}cute {H}ypoxia {E}xposure on the
{A}vailability of {A}1 {A}denosine {R}eceptors and
{P}erfusion in the {H}uman {B}rain.},
journal = {Journal of nuclear medicine},
volume = {66},
number = {1},
issn = {0097-9058},
address = {New York, NY},
publisher = {Soc.},
reportid = {DZNE-2025-00047},
pages = {142 - 149},
year = {2025},
abstract = {In 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.},
keywords = {Humans / Male / Receptor, Adenosine A1: metabolism / Adult
/ Brain: diagnostic imaging / Brain: metabolism / Brain:
blood supply / Female / Positron-Emission Tomography /
Cerebrovascular Circulation / Hypoxia: metabolism / Hypoxia:
physiopathology / Hypoxia: diagnostic imaging / Young Adult
/ Xanthines / Magnetic Resonance Imaging / A1AR (Other) /
ASL (Other) / PET (Other) / [18F]CPFPX (Other) / adenosine
receptors (Other) / hypoxia (Other) / Receptor, Adenosine A1
(NLM Chemicals) / Xanthines (NLM Chemicals) /
8-cyclopenta-3-(3-fluoropropyl)-1-propylxanthine (NLM
Chemicals)},
cin = {AG Boecker},
ddc = {610},
cid = {I:(DE-2719)1011202},
pnm = {353 - Clinical and Health Care Research (POF4-353)},
pid = {G:(DE-HGF)POF4-353},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:39667818},
doi = {10.2967/jnumed.124.268455},
url = {https://pub.dzne.de/record/274066},
}