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| Home > Publications database > Cerebral A(1) adenosine receptors (A(1)AR) in liver cirrhosis |
| Home > Publications database > Cerebral A(1) adenosine receptors (A(1)AR) in liver cirrhosis |
| Journal Article | PreJuSER-61611 |
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2008
Springer-Verl.
Heidelberg [u.a.]
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Please use a persistent id in citations: doi:10.1007/s00259-007-0586-z
Abstract: The cerebral mechanisms underlying hepatic encephalopathy (HE) are poorly understood. Adenosine, a neuromodulator that pre- and postsynaptically modulates neuronal excitability and release of classical neurotransmitters via A(1) adenosine receptors (A(1)AR), is likely to be involved. The present study investigates changes of cerebral A(1)AR binding in cirrhotic patients by means of positron emission tomography (PET) and [(18)F]CPFPX, a novel selective A(1)AR antagonist.PET was performed in cirrhotic patients (n = 10) and healthy volunteers (n = 10). Quantification of in vivo receptor density was done by Logan's non-invasive graphical analysis (pons as reference region). The outcome parameter was the apparent binding potential (aBP, proportional to B (max)/K (D)).Cortical and subcortical regions showed lower A(1)AR binding in cirrhotic patients than in controls. The aBP changes reached statistical significance vs healthy controls (p < 0.05, U test with Bonferroni-Holm adjustment for multiple comparisons) in cingulate cortex (-50.0%), precentral gyrus (-40.9%), postcentral gyrus (-38.6%), insular cortex (-38.6%), thalamus (-32.9%), parietal cortex (-31.7%), frontal cortex (-28.6), lateral temporal cortex (-28.2%), orbitofrontal cortex (-27.9%), occipital cortex (-24.6), putamen (-22.7%) and mesial temporal lobe (-22.4%).Regional cerebral adenosinergic neuromodulation is heterogeneously altered in cirrhotic patients. The decrease of cerebral A(1)AR binding may further aggravate neurotransmitter imbalance at the synaptic cleft in cirrhosis and hepatic encephalopathy. Different pathomechanisms may account for these alterations including decrease of A(1)AR density or affinity, as well as blockade of the A(1)AR by endogenous adenosine or exogenous xanthines.
Keyword(s): Adult (MeSH) ; Aged (MeSH) ; Brain: metabolism (MeSH) ; Brain: radionuclide imaging (MeSH) ; Female (MeSH) ; Humans (MeSH) ; Liver Cirrhosis: metabolism (MeSH) ; Liver Cirrhosis: radionuclide imaging (MeSH) ; Male (MeSH) ; Middle Aged (MeSH) ; Radiopharmaceuticals: diagnostic use (MeSH) ; Radiopharmaceuticals: pharmacokinetics (MeSH) ; Receptor, Adenosine A1: metabolism (MeSH) ; Tissue Distribution (MeSH) ; Xanthines: diagnostic use (MeSH) ; Xanthines: pharmacokinetics (MeSH) ; 8-cyclopenta-3-(3-fluoropropyl)-1-propylxanthine ; Radiopharmaceuticals ; Receptor, Adenosine A1 ; Xanthines ; J ; cirrhosis (auto) ; brain receptors and neurotransmitters (auto) ; positron emission tomography (auto) ; adenosine (auto) ; [F-18]CPFPX (auto)
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