Background And Aim: Imaging noradrenergic uptake in the liver with norepinephrine analog I-meta-iodobenzylguanidine (mIBG) was explored in normal controls and patients with heart failure (HF).
Methods: A total of 961 HF (343 with diabetes mellitus [DM]) and 94 control subjects underwent anterior planar mIBG images including upper abdomen at 15 min (early) and 3 h 50 min (late) post-injection. Decay-corrected liver activity normalized to injected activity and body surface area (counts/pixel [cpp]/MBq/m ) was compared in three groups: HF with DM; HF without DM; and controls. Associations with plasma norepinephrine, liver function tests, and level of cardiac innervation were explored.
Results: In controls, liver mIBG activity decreased over time (early: 2.78 vs late: 2.43 cpp/MBq/m , P < 0.0001); in HF subjects, activity increased during this interval (HF without DM: 2.85 vs 2.93 [P = 0.005]; HF with DM: 2.37 vs 2.43 [P = 0.054]). Early liver activity was lower in HF with DM subjects than in the other groups (P < 0.001); late liver activity was higher in HF without DM than in the other two groups (P < 0.01). Subjects with elevated plasma norepinephrine (> 520 pg/mL) or ≥ 1 abnormal liver function test had lower early and late liver activity. In subjects with preserved cardiac mIBG uptake, HF subjects had higher and control subjects lower liver activity than comparable subjects with decreased cardiac innervation.
Conclusions: In HF subjects, liver mIBG activity increased over time, reversing the normal washout pattern, suggesting a compensatory change in sympathetic nerve function. DM, abnormal liver function tests, and decreased cardiac innervation were associated with decreased liver mIBG uptake in HF.
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http://dx.doi.org/10.1111/jgh.15096 | DOI Listing |
Br J Pharmacol
December 2024
Laboratory of Molecular Pharmacology, HUN-REN Institute of Experimental Medicine, Budapest, Hungary.
Behav Brain Res
August 2024
Department of Neurology, BG University Hospital Bergmannsheil, Ruhr University Bochum, Germany.
The tendency to show the renewal effect of extinction appears as an intra-individually stable, reproducible processing strategy associated with differential patterns of BOLD activation in hippocampus, iFG and vmPFC, as well as differential resting-state functional connectivity between prefrontal regions and the dorsal attention network. Also, pharmacological modulations of the noradrenergic system that influence attentional processing have partially different effects upon individuals with (REN) and without (NoREN) a propensity for renewal. However, it is as yet unknown whether REN and NoREN individuals differ regarding microstructural properties in attention-related white matter (WM) regions, and whether such differences are related to noradrenergic processing.
View Article and Find Full Text PDFExpert Rev Neurother
August 2024
Department of Clinical and Experimental Medicine, University Hospital of Pisa, Pisa, Italy.
Introduction: Stimulants, including methylphenidate and amphetamines, are the first-line pharmacological treatment of ADHD in adults. However, in patients who do not respond or poorly tolerate stimulants, non-stimulant medications are usually recommended.
Areas Covered: The authors provide a narrative review of the literature on non-stimulant treatments for adult ADHD, including controlled and observational clinical studies conducted on adult samples.
Acta Physiol (Oxf)
August 2024
Department of Psychology, Trinity College Institute of Neuroscience, Trinity College Dublin, Dublin, Ireland.
Aim: Physical activity (PA) is a key component for brain health and Reserve, and it is among the main dementia protective factors. However, the neurobiological mechanisms underpinning Reserve are not fully understood. In this regard, a noradrenergic (NA) theory of cognitive reserve (Robertson, 2013) has proposed that the upregulation of NA system might be a key factor for building reserve and resilience to neurodegeneration because of the neuroprotective role of NA across the brain.
View Article and Find Full Text PDFHypertension
July 2024
Division of Clinical Pharmacology, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN (N.M., C.A.S.).
The NET (norepinephrine transporter) is situated in the prejunctional plasma membrane of noradrenergic neurons. It is responsible for >90% of the norepinephrine uptake that is released in the autonomic neuroeffector junction. Inhibitors of this cell membrane transporter, known as norepinephrine reuptake inhibitors (NRIs), are commercially available for the treatment of depression and attention deficit hyperactivity disorder.
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