scholarly journals Nucleoside transport inhibitor, dipyridamole, induced myocardial protection following hemorrhagic shock in ex vivo perfused rat hearts

2011 ◽  
Vol 23 (2) ◽  
pp. 75-80 ◽  
Author(s):  
Mona Soliman
Keyword(s):  
Hemorrhagic Shock ◽  
Myocardial Protection ◽  
Ex Vivo ◽  
Nucleoside Transport ◽  
Transport Inhibitor ◽  
Rat Hearts ◽  
Perfused Rat Hearts ◽  
Nucleoside Transport Inhibitor

scholarly journals An Advanced in Silico Modelling of the Interaction between FSCPX, an Irreversible A1 Adenosine Receptor Antagonist, and NBTI, a Nucleoside Transport Inhibitor, in the Guinea Pig Atrium

Molecules ◽  
2019 ◽  
Vol 24 (12) ◽  
pp. 2207 ◽  
Author(s):  
Adrienn Monika Szabo ◽  
Tamas Erdei ◽  
Gabor Viczjan ◽  
Rita Kiss ◽  
Judit Zsuga ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Adenosine Receptor ◽  
In Silico ◽  
Ex Vivo ◽  
Nucleoside Transport ◽  
A1 Adenosine Receptor ◽  
Adenosine Receptor Antagonist ◽  
Transport Inhibitor ◽  
Guinea Pig Atrium ◽  
Nucleoside Transport Inhibitor

In earlier studies, we generated concentration-response (E/c) curves with CPA (N6-cyclopentyladenosine; a selective A1 adenosine receptor agonist) or adenosine, in the presence or absence of S-(2-hydroxy-5-nitrobenzyl)-6-thioinosine (NBTI, a selective nucleoside transport inhibitor), and with or without a pretreatment with 8-cyclopentyl-N3-[3-(4-(fluorosulfonyl)-benzoyloxy)propyl]-N1-propylxanthine (FSCPX, a chemical known as a selective, irreversible A1 adenosine receptor antagonist), in isolated, paced guinea pig left atria. Meanwhile, we observed a paradoxical phenomenon, i.e., the co-treatment with FSCPX and NBTI appeared to enhance the direct negative inotropic response to adenosine. In the present in silico study, we aimed to reproduce eight of these E/c curves. Four models (and two additional variants of the last model) were constructed, each one representing a set of assumptions, in order to find the model exhibiting the best fit to the ex vivo data, and to gain insight into the paradoxical phenomenon in question. We have obtained in silico evidence for an interference between effects of FSCPX and NBTI upon our ex vivo experimental setting. Regarding the mechanism of this interference, in silico evidence has been gained for the assumption that FSCPX inhibits the effect of NBTI on the level of endogenous (but not exogenous) adenosine. As an explanation, it may be hypothesized that FSCPX inhibits an enzyme participating in the interstitial adenosine formation. In addition, our results suggest that NBTI does not stop the inward adenosine flux in the guinea pig atrium completely.

scholarly journals Antioxidant Solution in Combination with Angiotensin-(1-7) Provides Myocardial Protection in Langendorff-Perfused Rat Hearts

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Michaela Andrä ◽  
Miriam Russ ◽  
Susanne Jauk ◽  
Mariana Lamacie ◽  
Ingrid Lang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Myocardial Protection ◽  
Ischemia Reperfusion Injury ◽  
Organ Procurement ◽  
Ischemia Reperfusion ◽  
Morphological Alteration ◽  
Organ Shortage ◽  
Cold Ischemia ◽  
Rat Hearts ◽  
Perfused Rat Hearts

As progressive organ shortage in cardiac transplantation demands extension of donor criteria, effort is needed to optimize graft survival. Reactive oxygen and nitrogen species, generated during organ procurement, transplantation, and reperfusion, contribute to acute and late graft dysfunction. The combined application of diverse substances acting via different molecular pathways appears to be a reasonable approach to face the complex mechanism of ischemia reperfusion injury. Thus, an antioxidant solution containing α-ketoglutaric acid, 5-hydroxymethylfurfural, N-acetyl-L-methionine, and N-acetyl-selenium-L-methionine was combined with endogenous angiotensin-(1-7). Its capacity of myocardial protection was investigated in isolated Langendorff-perfused rat hearts subjected to warm and cold ischemia. The physiological cardiac parameters were assessed throughout the experiments. Effects were evaluated via determination of the oxidative stress parameters malondialdehyde and carbonyl proteins as well as immunohistochemical and ultrastructural tissue analyses. It was shown that a combination of 20% (v/v) antioxidant solution and 220 pM angiotensin-(1-7) led to the best results with a preservation of heart tissue against oxidative stress and morphological alteration. Additionally, immediate cardiac recovery (after warm ischemia) and normal physiological performance (after cold ischemia) were recorded. Overall, the results of this study indicate substantial cardioprotection of the novel combination with promising prospective for future clinical use.

Prevention of Catecholamine-Induced Cardiac Damage and Death with a Nucleoside Transport Inhibitor

1992 ◽  
Vol 20 (2) ◽  
pp. 173-178 ◽  
Author(s):  
Herman Van Belle ◽  
Willy Verheyen ◽  
Kris Ver Donck ◽  
Paul A. J. Janssen ◽  
J. Ian S. Robertson
Keyword(s):  
Nucleoside Transport ◽  
Cardiac Damage ◽  
Transport Inhibitor ◽  
Nucleoside Transport Inhibitor

Normalization strategy is critical for the outcome of miRNA expression analyses in the rat heart

2011 ◽  
Vol 43 (10) ◽  
pp. 604-610 ◽  
Author(s):  
Trond Brattelid ◽  
Eva-Katrine Aarnes ◽  
Erik Helgeland ◽  
Steinar Guvaåg ◽  
Heike Eichele ◽  
...  
Keyword(s):  
Mirna Expression ◽  
Rat Heart ◽  
Ex Vivo ◽  
Rank Order ◽  
Free Water ◽  
Early Reperfusion ◽  
Rat Hearts ◽  
Perfused Rat Hearts ◽  
Assay Protocol ◽  
4.5S Rna

Since normalization strategies plays a pivotal role for obtaining reliable results when performing quantitative PCR (qPCR) analyses, this study investigated several miRNA normalization candidates in regards to their efficiency as normalization standards in the ischemic reperfused ex vivo rat heart, with special reference to regulation of the miRNAs miR-1 and miR-101b. The possibility of including primers for several miRNAs in one reverse transcription (RT) reaction was also investigated. Langendorff perfused rat hearts were subjected to 30 min regional ischemia and 0, 1, 5, 15, or 120 min reperfusion. Total RNA was isolated and reverse transcribed for miRNA qPCR analysis. Normalization candidates were evaluated by the NormFinder and geNorm algorithms and the following stability expression rank order was obtained: sno202 < U6B < U87 < snoRNA < 4.5S RNA A < Y1 < 4.5S RNA B < GAPDH. Applying U6B as a normalizer it was found that miR-1 and miR-101b was downregulated in the ischemic reperfused myocardium. Furthermore, up to three primers could be included in one RT reaction by replacing RNase-free water with two supplemental sets of primers in the TaqMan MicroRNA assay protocol. This study demonstrates the importance of validating normalization standards when performing miRNA expression analyses by qPCR, and that miR-1 and miR-101b may play an important role during early reperfusion of the ischemic rat heart.

Myocardial protection and esmolol in blood perfused rat hearts

2006 ◽  
Vol 40 (6) ◽  
pp. 956-957
Author(s):  
M. Fujii ◽  
M. Kambe ◽  
Y. Maruyama ◽  
D. Nishina ◽  
R. Bessho ◽  
...  
Keyword(s):  
Myocardial Protection ◽  
Rat Hearts ◽  
Perfused Rat Hearts

scholarly journals The 2-chlorodeoxyadenosine-induced cell death signalling pathway in human thymocytes is different from that induced by 2-chloroadenosine

1995 ◽  
Vol 311 (2) ◽  
pp. 585-588 ◽  
Author(s):  
Z Szondy
Keyword(s):  
Cell Death ◽  
Nucleoside Transport ◽  
Signalling Pathways ◽  
Deoxycytidine Kinase ◽  
Induce Cell Death ◽  
Kinase C ◽  
Transport Inhibitor ◽  
Dependent Cell ◽  
Nucleoside Transport Inhibitor ◽  
Induced Apoptosis

2-chloroadenosine induced DNA fragmentation and cell death in human thymocytes primarily by Ca(2+)-dependent mechanisms. Incubation of human thymocytes with 2-chlorodeoxyadenosine (5-1000 nM) also induced cell death (apoptosis) which was dependent on macromolecule synthesis and involved activation of an endonuclease which was inhibited by Zn2+. The effect of 2-chlorodeoxyadenosine was prevented by addition of dipyridamole, a strong nucleoside transport inhibitor, or of deoxycytidine, previously shown to compete for uptake by deoxycytidine kinase. 2-Chlorodeoxyadenosine-induced apoptosis did not involve increases in the cytosolic Ca2+ concentration, but required the presence of intracellular Ca2+. It was not inhibited by activators of protein kinase C previously shown to inhibit Ca(2+)-dependent cell death. Addition of 2-chlorodeoxyadenosine induced an increase in the amount of p53 in human thymocytes, while 2-chloroadenosine had no effect. These data suggest that 2-chloroadenosine and 2-chlorodeoxyadenosine induce cell death in human thymocytes via different signalling pathways.

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