Norepinephrine Evoked by Potassium Depolarization Increases Interstitial Adenosine Concentration via Activation of ecto-5′-Nucleotidase in Rat Hearts

2003 ◽  
Vol 305 (2) ◽  
pp. 719-724 ◽  
Author(s):  
Toshio Obata ◽  
Hidetoshi Yonemochi ◽  
Makoto Arita
Keyword(s):  
Potassium Depolarization ◽  
Rat Hearts ◽  
Adenosine Concentration

Transcapillary adenosine transport in isolated guinea pig and rat hearts

1990 ◽  
Vol 259 (3) ◽  
pp. H772-H783 ◽  
Author(s):  
D. E. Mohrman ◽  
L. J. Heller
Keyword(s):  
Endothelial Cells ◽  
Guinea Pig ◽  
Surface Area ◽  
High Performance ◽  
Cell Metabolism ◽  
Rat Hearts ◽  
Permeability Surface ◽  
Adenosine Concentration ◽  
Adenosine Transport ◽  
Area Product

Transcapillary adenosine transport was studied in isolated guinea pig and rat hearts perfused with a colloid-free solution. High-performance liquid chromatography techniques were used to measure adenosine concentration of venous and interstitial (epicardial surface) fluid during steady-state perfusion with various concentrations of adenosine. A mathematical model was used to analyze these data to obtain estimates of the following parameters of transcapillary adenosine transport: PSg, permeability-surface area product for adenosine movement through interendothelial cell channels; PSecl, permeability-surface area product for adenosine movement through the luminal plasma membrane of endothelial cells; and Gec, clearance rate constant for endothelial cell metabolism and/or sequestration of adenosine. In both guinea pig and rat hearts, PSg was estimated to be less than or equal to 3 ml.min-1.g-1. Estimates of PSecl and Gec of guinea pig hearts (7.2 +/- 0.4 and 230 +/- 157 ml.min-1.g-1) were significantly less than those of rat hearts (66 +/- 11 and 2,490 +/- 1,360 ml.min-1.g-1). That PSecl is greater than PSg in both species indicates that endothelial cells represent an important pathway for transcapillary adenosine transport. That Gec is much greater than PSecl in both species implies that endothelial cells act as a sink for adenosine from surrounding areas. Our results indicate that endothelium is a stronger sink for adenosine in rat hearts than in guinea pig hearts. Inosine infusion (10(-4)M) had little effect on the estimated PSecl and Gec in guinea pig hearts but reduced these parameters several-fold in rat hearts, suggesting that different transport mechanisms for adenosine exist in endothelia of guinea pig and rat hearts.

Iron storage sites in the myocardium as revealed by cytohistochemistry

1988 ◽  
Vol 46 ◽  
pp. 394-395
Author(s):  
M. Ashraf ◽  
F. Thompson ◽  
S. Miki ◽  
P. Srivastava
Keyword(s):  
Cardiac Tissue ◽  
Coronary Perfusion ◽  
Intracellular Iron ◽  
Ether Anesthesia ◽  
Intense Staining ◽  
Iron Storage ◽  
Thin Sections ◽  
Rat Hearts ◽  
Cacodylate Buffer ◽  
Made In

Iron is believed to play an important role in the pathogenesis of ischemic injury. However, the sources of intracellular iron in myocytes are not yet defined. In this study we have attempted to localize iron at various cellular sites of the cardiac tissue with the ferrocyanide technique.Rat hearts were excised under ether anesthesia. They were fixed with coronary perfusion with 3% buffered glutaraldehyde made in 0.1 M cacodylate buffer pH 7.3. Sections, 60 μm in thickness, were cut on a vibratome and were incubated in the medium containing 500 mg of potassium ferrocyanide in 49.5 ml H2O and 0.5 ml concentrated HC1 for 30 minutes at room temperature. Following rinses in the buffer, tissues were dehydrated in ethanol and embedded in Spurr medium.The examination of thin sections revealed intense staining or reaction product in peroxisomes (Fig. 1).

Blood cardioplegia: Difference between young and old rat hearts

2013 ◽  
Vol 61 (S 01) ◽  
Author(s):  
L Kohlhepp ◽  
B Niemann ◽  
M Heep ◽  
S Rohrbach ◽  
KD Schlüter ◽  
...  
Keyword(s):  
Blood Cardioplegia ◽  
Rat Hearts

Mechanism of the Antiplatelet Action of Dipyridamole in Whole Blood: Modulation of Adenosine Concentration and Activity

1986 ◽  
Vol 55 (01) ◽  
pp. 012-018 ◽  
Author(s):  
Paolo Gresele ◽  
Jef Arnout ◽  
Hans Deckmyn ◽  
Jos Vermylen
Keyword(s):  
Platelet Aggregation ◽  
Adenosine Receptor ◽  
Whole Blood ◽  
Blood Cells ◽  
Inhibitory Action ◽  
Phosphodiesterase Inhibitor ◽  
Inhibitory Effect ◽  
Adenosine Concentration ◽  
Pharmacological Studies

SummaryDipyridamole inhibits platelet aggregation in whole blood at lower concentrations than in plasma. The blood cells responsible for increased effectiveness in blood are the erythrocytes. Using the impedance aggregometer we have carried out a series of pharmacological studies in vitro to elucidate the mechanism of action of dipyridamole in whole blood. Adenosine deaminase, an enzyme breaking down adenosine, reverses the inhibitory action of dipyridamole. Two different adenosine receptor antagonists, 5’-deoxy-5’-methylthioadenosine and theophylline, also partially neutralize the activity of dipyridamole in blood. Enprofylline, a phosphodiesterase inhibitor with almost no adenosine receptor antagonistic properties, potentiates the inhibition of platelet aggregation by dipyridamole. An inhibitory effect similar to that of dipyridamole can be obtained combining a pure adenosine uptake inhibitor (RE 102 BS) with a pure phosphodiesterase inhibitor (MX-MB 82 or enprofylline). Mixing the blood during preincubation with dipyridamole increases the degree of inhibition. Lowering the haematocrit slightly reduces the effectiveness.Although we did not carry out direct measurements of adenosine levels, the results of our pharmacological studies clearly show that dipyridamole inhibits platelet aggregation in whole blood by blocking the reuptake of adenosine formed from precursors released by red blood cells following microtrauma. Its slight phosphodiesterase inhibitory action potentiates the effects of adenosine on platelets.

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