scholarly journals Protective effects of adenosine A2A receptor agonist in ventilator-induced lung injury in rats

2009 ◽  
Vol 37 (7) ◽  
pp. 2235-2241 ◽  
Author(s):  
Chin-Ming Chen ◽  
Oscar Penuelas ◽  
Kieran Quinn ◽  
Kuo-Chen Cheng ◽  
Chien-Feng Li ◽  
...  

2019 ◽  
Vol 4 (2) ◽  
pp. 1-10 ◽  
Author(s):  
Anna Dons-Jensen ◽  
Line Petersen ◽  
Hans-Erik Bøtker ◽  
Toke Bek

Background: The neurotransmitter adenosine has been proposed to be involved in the pathogenesis of diabetic retinopathy, which may be due to the vasoactive properties of the compound. Previous studies have shown that adenosine can affect the tone of retinal arterioles in vitro to induce dilatation mediated by A2A and A2Breceptors and constriction mediated by A1 and A3 receptors. Purpose: To investigate effects of intravenous administration of the adenosine A2A receptor agonist regadenoson on the diameter of retinal vessels in vivo. Method: The diameter responses of larger retinal arterioles and venules were evaluated using the dynamic vessel analyser in 20 normal persons (age 22–31 years) after intravenous administration of the adenosine A2A receptor agonist regadenoson during exposure to systemic normoxia and hypoxia. Results: The diameter of retinal arterioles and venules increased significantly during stimulation with flickering light (p < 0.0001). Regadenoson reduced the flicker-induced dilatation of venules during normoxia (p = 0.0006), but otherwise had no effect on vessel diameters (p > 0.08 for all comparisons). Conclusions:Intravenous administration of the adenosine A2A receptor agonist regadenoson had no significant effect on the diameter of retinal arterioles. Future studies should investigate differential effects of intra- and extravascular administration of adenosine receptor agonists on retinal vessels.



2002 ◽  
Vol 438 (3) ◽  
pp. 183-188 ◽  
Author(s):  
John R Fozard ◽  
Karen M Ellis ◽  
Maria F Villela Dantas ◽  
Bruno Tigani ◽  
Lazzaro Mazzoni




2006 ◽  
Vol 45 (12) ◽  
pp. 1201-1212 ◽  
Author(s):  
Toufigh Gordi ◽  
Paul Frohna ◽  
Hai-Ling Sun ◽  
Andrew Wolff ◽  
Luiz Belardinelli ◽  
...  


2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Byeong Woo KIm ◽  
Sun hee Kim ◽  
Ki beom Bae

Abstract Background and Aims We demonstrate the marked activity of SW033291, an inhibitor of 15-hydoxyprostaglandin dehydrogenase (15-PGDH), in preventing acute kidney injury (AKI) in a murine model of ischemia reperfusion injury (IRI). AKI due to ischemic injury represents a significant clinical problem. Prostaglandin E2 (PGE2) is vasodilator in the kidney, but is rapidly degraded in vivo due to catabolism by 15-PGDH. We investigated the potential of SW033291, a potent and specific 15-PGDH inhibitor, as prophylactic treatment for ischemic AKI. Method 10-week aged male C57/BL6 mice were randomly allocated to five groups (n=8 to 15 in each group): the sham-control group, sham-SW033291 group, IRI-vehicle group, IRI-indomethacin group and the IRI-SW033291 group. IRI were induced by clamping bilateral renal artery for 30 min followed by 24 hours of reperfusion. Vehicle, indomethacin, or SW033291 were intraperitoneally administered three times at 1 hour before, immediately after, and 12 hours after IRI. Renal function, histological changes, and renal blood flow were compared and the relevant parameters of oxidative stress and inflammation were detected. Results Prophylactic administration of SW033291 significantly increased renal tissue PGE2 levels and increased post-AKI renal blood flow and renal arteriole area. In parallel, prophylactic SW033291 decreased post-AKI histologic injury score and tubular apoptosis and markedly reduced biomarkers of renal injury that included BUN, creatinine, NGAL and KIM-1. Prophylactic SW033291 also reduced post-AKI induction of proinflammatory cytokines, high mobility group box 1 (HMGB1), and malondialdehyde (MDA). Protective effects of SW033291 were mediated by PGE2 signaling as they could be blocked by pharmacologic inhibition of PGE2 synthesis or of the EP4 type PGE2 receptor. Consistent with activation of PGE2 signaling, SW033291 induced renal levels of both EP4 and of cyclic adenosine monophosphate (cAMP), along with other vasodilatory effectors including AMP, adenosine, and the adenosine A2A receptor (A2A). Protective effects of SW0333291 could largely be achieved with a single prophylactic dose of the drug. Conclusion Inhibiting 15-PGDH may thus represent a novel strategy for prophylaxis of ischemic AKI in multiple clinical settings, including renal transplantation and cardiovascular surgery.



2006 ◽  
Vol 34 (4) ◽  
pp. 1119-1125 ◽  
Author(s):  
György Haskó ◽  
Da-Zhong Xu ◽  
Qi Lu ◽  
Zoltán H. Németh ◽  
Jondavid Jabush ◽  
...  


2012 ◽  
Vol 28 (1) ◽  
pp. 45-52 ◽  
Author(s):  
Fatemeh Kermanian ◽  
Mansooreh Soleimani ◽  
Alireza Ebrahimzadeh ◽  
Hossein Haghir ◽  
Mehdi Mehdizadeh


ChemInform ◽  
2010 ◽  
Vol 31 (10) ◽  
pp. no-no
Author(s):  
David R. Borcherding ◽  
Nelsen L. Lentz ◽  
Philip M. Weintraub ◽  
Mark W. Dudley ◽  
Roberta Secrest ◽  
...  


PLoS ONE ◽  
2018 ◽  
Vol 13 (4) ◽  
pp. e0195047 ◽  
Author(s):  
Allan K. Alencar ◽  
Fábio I. Carvalho ◽  
Ananssa M. Silva ◽  
Sabrina T. Martinez ◽  
Jorge A. Calasans-Maia ◽  
...  


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