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SPECT/microSPECT Imaging
Published in Robert J. Gropler, David K. Glover, Albert J. Sinusas, Heinrich Taegtmeyer, Cardiovascular Molecular Imaging, 2007
Lars R. Furenlid, Zhonglin Liu, Harrison H. Barrett
Adenosine has been recognized to be one of mediators involved in IPC cardioprotection by stimulating the adenosine A1 receptor. The vasodilatation of adenosine-mediating IPC has been extensively described in a variety of animal models (25,26). However, for rat hearts such a role is controversial. We hypothesized that the adenosine A1 receptor is involved in protection by IPC, in which case a receptor agonist, 2-chloro-N6-cyclopentyladenosine (CCPA), should give a protection similar to IPC, while the receptor antagonist, 8-(p-sulfophenyl)-theophylline (SPT), should block protection by IPC. We quantified the kinetic washout of 99mTc-glucarate from the ischemic-reperfused zone and normal myocardium in rat hearts subjected to varied treatments. The hot spot of 99mTc-glucarate showed significantly higher fractional washout in the heart with IPC and CCPA compared to the control heart without IPC (No-IPC) and SPT. As a result, the hot spots in IPC and CCPA exhibited significantly lower radioactive retention (% peak) than in No-IPC and SPT, respectively (see Fig. 10). The hot spots in CCPA demonstrated similar radioactive retention as in IPC. The increased hot-spot retention in the SPT hearts was as high as in the No-IPC heart. Our data indicate that cardioprotection by IPC could be simulated by the adenosine receptor agonist CCPA, or blocked by the antagonist SPT.
Caffeine in the modulation of brain function
Published in B.S. Gupta, Uma Gupta, Caffeine and Behavior, 2020
J. Patrick Myers, David A. Johnson, Devon E. McVey
The effects of caffeine on brain acetylcholine have not been studied as thoroughly as those of other neurotransmitters. The effects of caffeine on acetylcholine in electrically stimulated brain slices varies as a function of caffeine concentration and frequency of stimulation.12 Additionally, caffeine and theophylline have been shown to increase acetylcholine outflow from the cerebral cortex of anesthetized rats with the IP administration of 15 and 30 mg/kg.58 Intracerebral injection of theophylline has also been shown to increase acetylcholine turn-over in the hippocampus of rats.52 More recent studies have shown the concentration of acetylcholine to be increased in the striatum of anesthetized rats after IP administration of combinations of caffeine and choline at doses of 50 mg/kg caffeine and 120 mg/kg choline.59 Carter et al.,60 following oral administration of caffeine (3 to 30 mg/kg), found a significant rise in extracellular levels of acetylcholine in the hippocampus of conscious rats. This increase could be blocked when the microdialysis probe was perfused with tetrodotoxin or the A1-receptor agonist, N6-cyclopentyladenosine, but not the A2-receptor agonist CGS 21680. This study, therefore, suggested that orally administered caffeine produced its effect via blockade of A1-receptors. In support of these findings, Shi et al.61 found that chronic ingestion of caffeine by mice leads to a significant increase in A1-adenosine receptors. Others, however, have found that chronic consumption of high doses of caffeine reduces the effect of caffeine on cortical acetylcholine release, an effect which is independent of adenosine.54
Novel and emerging therapeutics for genetic epilepsies
Published in Expert Review of Neurotherapeutics, 2021
Ana Pejčić, Slobodan M. Janković, Miralem Đešević, Refet Gojak, Snežana Lukić, Nenad Marković, Miloš Milosavljević
Adenosine-Augmentation Therapies using adenosine kinase (ADK) inhibitors or adenosine A1 receptor agonists may be a novel therapy for refractory epilepsy caused by Sturge-Weber syndrome, considering that it has been shown that brain tissues from these patients show overexpression of ADK in glial cells [162,163]. Results of an in vitro electrophysiological study on human brain tissue taken from patients with Sturge-Weber syndrome showed that adenosine A1 receptor agonist Chloro-N6-cyclopentyladenosine (CCPA) decreased the excitability of fast-spiking interneurons, which suggested that it may be beneficial for reducing life burden in patients with refractory epilepsy in Sturge-Weber syndrome, with application to epileptic generation region, but not to propagation region [162].
Istradefylline, an adenosine A2a receptor antagonist, inhibits the CD4+ T-cell hypersecretion of IL-17A and IL-8 in humans
Published in Immunological Medicine, 2022
Mieko Tokano, Masaaki Kawano, Rie Takagi, Sho Matsushita
CD4+ T cells or PBMCs (1.5 × 105 cells/well of 96-well plates) were stimulated for 3 days at 37 °C with anti-human CD3 (BioLegend, San Diego, CA, USA; 5 μg/mL) and CD28 (BioLegend; 1 μg/mL) antibodies (Abs) (CD3/CD28) in the presence of adenosine (0–300 μM), an A2aR antagonist (istradefylline; Sigma-Aldrich; 0–10 nM) plus adenosine (100 μM), and adenosine receptor agonists (0–10 μM) (A1R: 2-Chloro-N6-cyclopentyladenosine [CCPA], Tocris, Bristol, UK; A2aR: PSB0777, Tocris; A2bR: BAY 60-6583, Tocris; A3R: HEMADO, Tocris) in 200 μL of R10H medium. After stimulation, the supernatants were collected for use in cytokine ELISAs.
The Toxic Effects of Ethylene Glycol Tetraacetate Acid, Ferrum Lek and Methanol on the Glutathione System: correction Options
Published in Expert Review of Clinical Pharmacology, 2021
The EGTA administration was fraught with side effects, such as cardiac arrest and global cerebral ischemia. Golapel reported that EGTA has reduced the lifespan of mice to 34 sec after administration [20]. The combination of EGTA with CPA and lidocaine increased the life expectancy of animals to 2 min and 20 sec. However, only 37% of the mice survived. These data prove that N6-cyclopentyladenosine has a high protective effect.