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The Cardiovascular System
Published in Pritam S. Sahota, James A. Popp, Jerry F. Hardisty, Chirukandath Gopinath, Page R. Bouchard, Toxicologic Pathology, 2018
Calvert Louden, David Brott, Chidozie J. Amuzie, Bindu Bennet, Ronnie Chamanza
In non-human primates segmental, medial necrosis, and hemorrhage as well as inflammation and a fibroproliferative response were seen in the extramural coronary arteries following administration of an endothelin receptor antagonist (CI-1020), an anti-hypertensive adenosine receptor agonist or a PDE IV inhibitor (Albassam et al. 1999; Albassam et al. 1998). Standard measurement of HR and/or MAP did not reveal any major hemodynamic alterations, so mechanistically, the relationship between the vascular pathology seen in non-human primates and altered hemodynamics is not clear.
Application of Intracoronary Physiology: Use of Pressure and Flow Measurements
Published in Debabrata Mukherjee, Eric R. Bates, Marco Roffi, Richard A. Lange, David J. Moliterno, Nadia M. Whitehead, Cardiovascular Catheterization and Intervention, 2017
Morton J. Kern, Arnold H. Seto
Regadenoson is an a2A adenosine receptor agonist that induces coronary vasodilatation and increases myocardial blood flow in a manner reportedly equivalent to adenosine with fewer adverse effects. Regadenoson has a halflife of 2-3 minutes in the initial phase, 30 minutes in the intermediate phase, and 2 hours in the terminal phase. It is administered as single intravenous bolus (0.4 mg), and thus may be easier to use, but its cost and prolonged effect may complicate the measurement of multiple lesions or arteries.15, 16
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.
Efflux proteins at the blood–brain barrier: review and bioinformatics analysis
Published in Xenobiotica, 2018
Massoud Saidijam, Fatemeh Karimi Dermani, Sareh Sohrabi, Simon G. Patching
It is also apparent that the A2A adenosine receptor modulates P-gp at the blood–brain barrier. The A2A adenosine receptor agonist Lexiscan rapidly and potently decreased P-gp expression and function in a time-dependent and reversible manner, which coincided with drug accumulation in brains of wild-type mice and in primary mouse and human brain endothelial cells (Kim & Bynoe, 2016). A2A adenosine receptor activation at the blood–brain barrier could, therefore, be used to fine-tune drug delivery to the brain and has potential as a novel technology for drug delivery to the brain and central nervous system.
Defibrotide sodium for the treatment of hepatic veno-occlusive disease/sinusoidal obstruction syndrome
Published in Expert Review of Clinical Pharmacology, 2018
Paul G. Richardson, Brandon M. Triplett, Vincent T. Ho, Nelson Chao, Fiona L. Dignan, Michelle Maglio, Mohamad Mohty
In vitro, defibrotide has been shown to bind to various sites predominantly located on the plasma membranes of the vascular endothelium [44,46]. It acts as an adenosine receptor agonist and is thought to have affinity for receptors A1 and A2 [39], although a recent in vitro study was unable to find support for this interaction [46].