Inhibiting N-cadherin-mediated adhesion affects gap junction communication in isolated rat hearts

2010 ◽  
Vol 30 (3) ◽  
pp. 193-200 ◽  
Author(s):  
Hongjun Zhu ◽  
Hegui Wang ◽  
Xiwen Zhang ◽  
Xiaofeng Hou ◽  
Kejiang Cao ◽  
...  
Keyword(s):  
Gap Junction ◽  
Gap Junction Communication ◽  
Rat Hearts ◽  
Isolated Rat

Protective effect of gap junction uncouplers given during hypoxia against reoxygenation injury in isolated rat hearts

2006 ◽  
Vol 290 (2) ◽  
pp. H648-H656 ◽  
Author(s):  
Antonio Rodríguez-Sinovas ◽  
David García-Dorado ◽  
Marisol Ruiz-Meana ◽  
Jordi Soler-Soler
Keyword(s):  
Protective Effect ◽  
Gap Junction ◽  
Electrical Impedance ◽  
Palmitoleic Acid ◽  
Cell Injury ◽  
Glycyrrhetinic Acid ◽  
Response Analysis ◽  
Rat Hearts ◽  
Ldh Release ◽  
Isolated Rat

It has been shown that cell-to-cell chemical coupling may persist during severe myocardial hypoxia or ischemia. We aimed to analyze the effects of different, chemically unrelated gap junction uncouplers on the progression of ischemic injury in hypoxic myocardium. First, we analyzed the effects of heptanol, 18α-glycyrrhetinic acid, and palmitoleic acid on intracellular Ca2+ concentration during simulated hypoxia (2 mM NaCN) in isolated cardiomyocytes. Next, we analyzed their effects on developed and diastolic tension and electrical impedance in 47 isolated rat hearts submitted to 40 min of hypoxia and reoxygenation. All treatments were applied only during the hypoxic period. Cell injury was determined by lactate dehydrogenase (LDH) release. Heptanol, but not 18α-glycyrrhetinic acid nor palmitoleic acid, attenuated the increase in cytosolic Ca2+ concentration induced by simulated ischemia in cardiomyocytes and delayed rigor development (rigor onset at 7.31 ± 0.71 min in controls vs. 14.76 ± 1.44 in heptanol-treated hearts, P < 0.001) and the onset of the marked changes in electrical impedance (tissue resistivity: 4.02 ± 0.29 vs. 7.75 ± 1.84 min, P = 0.016) in hypoxic rat hearts. LDH release from hypoxic hearts was minimal and was not significantly modified by drugs. However, all gap junction uncouplers, given during hypoxia, attenuated LDH release during subsequent reoxygenation. Dose-response analysis showed that increasing heptanol concentration beyond the level associated with maximal effects on cell coupling resulted in further protection against hypoxic injury. In conclusion, gap junction uncoupling during hypoxia has a protective effect on cell death occurring upon subsequent reoxygenation, and heptanol has, in addition, a marked protective effect independent of its uncoupling actions.

Independent dual perfusion of left and right coronary arteries in isolated rat hearts

1991 ◽  
Vol 261 (6) ◽  
pp. H2082-H2090 ◽  
Author(s):  
M. Avkiran ◽  
M. J. Curtis
Keyword(s):  
High Energy ◽  
Low Flow ◽  
Blue Dye ◽  
Ischemia And Reperfusion ◽  
Langendorff Preparation ◽  
Rat Hearts ◽  
Left And Right ◽  
Conventional Models ◽  
Aortic Cannula ◽  
Isolated Rat

A novel dual lumen aortic cannula was designed and constructed to permit independent perfusion of left and right coronary beds in isolated rat hearts without necessitating the cannulation of individual arteries. Stability of the dual-perfusion preparation was shown to be similar to that of the conventional Langendorff preparation, in terms of coronary flow, heart rate, and high-energy phosphate content. The independence of left and right perfusion beds was confirmed by unilateral infusion of disulfine blue dye and spectrophotometric detection of the dye in ventricular homogenates. Transient cessation of flow to the left coronary bed resulted in severe ventricular arrhythmias upon reperfusion, as in conventional models of regional ischemia and reperfusion. The dual-perfusion model is technically undemanding, reproducible, inexpensive, and can be used in several species. It enables studies with 1) regional low flow ischemia, 2) regional zero-flow ischemia without coronary ligation (with attendant damage to vasculature), 3) selective application of drugs or interventions to the ischemic-reperfused zone, and 4) selective application of components of ischemia and reperfusion to a site anatomically relevant to ischemic heart disease.

The Effects of Low-Flow Ischemia on K+Fluxes in Isolated Rat Hearts Assessed by87Rb NMR

1999 ◽  
Vol 31 (4) ◽  
pp. 817-826 ◽  
Author(s):  
V.V. Kupriyanov ◽  
B. Xiang ◽  
B. Kuzio ◽  
R. Deslauriers
Keyword(s):  
Low Flow ◽  
Rat Hearts ◽  
Isolated Rat

scholarly journals Attenuation of extracellular ATP response in cardiomyocytes isolated from hearts subjected to ischemia-reperfusion

2005 ◽  
Vol 289 (2) ◽  
pp. H614-H623 ◽  
Author(s):  
Harjot K. Saini ◽  
Vijayan Elimban ◽  
Naranjan S. Dhalla
Keyword(s):  
Cardiac Function ◽  
Positive Inotropic Effect ◽  
Ischemia Reperfusion ◽  
Cardiac Contractility ◽  
Extracellular Atp ◽  
Binding Characteristics ◽  
Rat Hearts ◽  
The Status ◽  
Intracellular Ca ◽  
Isolated Rat

Extracellular ATP is known to augment cardiac contractility by increasing intracellular Ca2+ concentration ([Ca2+]i) in cardiomyocytes; however, the status of ATP-mediated Ca2+ mobilization in hearts undergoing ischemia-reperfusion (I/R) has not been examined previously. In this study, therefore, isolated rat hearts were subjected to 10–30 min of global ischemia and 30 min of reperfusion, and the effect of extracellular ATP on [Ca2+]i was measured in purified cardiomyocytes by fura-2 microfluorometry. Reperfusion for 30 min of 20-min ischemic hearts, unlike 10-min ischemic hearts, revealed a partial depression in cardiac function and ATP-induced increase in [Ca2+]i; no changes in basal [Ca2+]i were evident in 10- or 20-min I/R preparations. On the other hand, reperfusion of 30-min ischemic hearts for 5, 15, or 30 min showed a marked depression in both cardiac function and ATP-induced increase in [Ca2+]i and a dramatic increase in basal [Ca2+]i. The positive inotropic effect of extracellular ATP was attenuated, and the maximal binding characteristics of 35S-labeled adenosine 5′-[γ-thio]triphosphate with crude membranes from hearts undergoing I/R was decreased. ATP-induced increase in [Ca2+]i in cardiomyocytes was depressed by verapamil and Cibacron Blue in both control and I/R hearts; however, this response in I/R hearts, unlike control hearts, was not affected by ryanodine. I/R-induced alterations in cardiac function and ATP-induced increase in [Ca2+]i were attenuated by treatment with an antioxidant mixture and by ischemic preconditioning. The observed changes due to I/R were simulated in hearts perfused with H2O2. The results suggest an impairment of extracellular ATP-induced Ca2+ mobilization in I/R hearts, and this defect appears to be mediated through oxidative stress.

Effect of cicletanine on ischemia/reperfusion-induced ion shifts in isolated rat hearts

1990 ◽  
Vol 22 ◽  
pp. S64
Author(s):  
Arpad Tosaki ◽  
Matyas Koltai ◽  
Thierry Tarrade ◽  
Pierre Braquet
Keyword(s):  
Ischemia Reperfusion ◽  
Rat Hearts ◽  
Ion Shifts ◽  
Isolated Rat
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