scholarly journals Anatomical Model of Rat Ventricles to Study Cardiac Arrhythmias under Infarction Injury

Mathematics ◽  
2021 ◽  
Vol 9 (20) ◽  
pp. 2604
Author(s):  
Roman Rokeakh ◽  
Tatiana Nesterova ◽  
Konstantin Ushenin ◽  
Ekaterina Polyakova ◽  
Dmitry Sonin ◽  
...  
Keyword(s):  
Cardiac Arrhythmias ◽  
Rat Heart ◽  
Ischemia Reperfusion ◽  
Spiral Wave ◽  
Myocardial Damage ◽  
Experimental System ◽  
Border Zone ◽  
Ionic Model ◽  
Cellular Models ◽  
Species Specific

Species-specific computer models of the heart are a novel powerful tool in studies of life-threatening cardiac arrhythmias. Here, we develop such a model aimed at studying infarction injury in a rat heart, the most common experimental system to investigate the effects of myocardial damage. We updated the Gattoni2016 cellular ionic model by fitting its parameters to experimental data using a population modeling approach. Using four selected cellular models, we studied 2D spiral wave dynamics and found that they include meandering and break-up. Then, using an anatomically realistic ventricular geometry and fiber orientation in the rat heart, we built a model with a post-infarction scar to study the electrophysiological effects of myocardial damage. A post-infarction scar was simulated as an inexcitable obstacle surrounded by a border zone with modified cardiomyocyte properties. For cellular models, we studied the rotation of scroll waves and found that, depending on the model, we can observe different types of dynamics: anchoring, self-termination or stable rotation of the scroll wave. The observed arrhythmia characteristics coincide with those measured in the experiment. The developed model can be used to study arrhythmia in rat hearts with myocardial damage from ischemia reperfusion and to examine the possible arrhythmogenic effects of various experimental interventions.

scholarly journals Inhibition of LINE-1 expression in the heart decreases ischemic damage by activation of Akt/PKB signaling

2006 ◽  
Vol 25 (2) ◽  
pp. 314-324 ◽  
Author(s):  
Eliana Lucchinetti ◽  
Jianhua Feng ◽  
Rafaela da Silva ◽  
Genrich V. Tolstonog ◽  
Marcus C. Schaub ◽  
...  
Keyword(s):  
Infarct Size ◽  
Functional Recovery ◽  
Rat Heart ◽  
Cardiac Tissue ◽  
Ischemia Reperfusion ◽  
Myocardial Damage ◽  
Immunoblot Analysis ◽  
Rat Hearts ◽  
Perfused Rat Hearts ◽  
Antisense Odns

Microarray analyses indicate that ischemic and pharmacological preconditioning suppress overexpression of the non-long terminal repeat retrotransposon long interspersed nuclear element 1 (LINE-1, L1) after ischemia-reperfusion in the rat heart. We tested whether L1 overexpression is mechanistically involved in postischemic myocardial damage. Isolated, perfused rat hearts were treated with antisense or scrambled oligonucleotides (ODNs) against L1 for 60 min and exposed to 40 min of ischemia followed by 60 min of reperfusion. Functional recovery and infarct size were measured. Effective nuclear uptake was determined by FITC-labeled ODNs, and downregulation of L1 transcription was confirmed by RT-PCR. Immunoblot analysis was used to assess changes in expression levels of the L1-encoded proteins ORF1p and ORF2p. Immunohistochemistry was performed to localize ORF1/2 proteins in cardiac tissue. Effects of ODNs on prosurvival protein kinase B (Akt/PKB) expression and activity were also determined. Antisense ODNs against L1 prevented L1 burst after ischemia-reperfusion. Inhibition of L1 increased Akt/PKBβ expression, enhanced phosphorylation of PKB at serine 473, and markedly improved postischemic functional recovery and decreased infarct size. Antisense ODN-mediated protection was abolished by LY-294002, confirming the involvement of the Akt/PKB survival pathway. ORF1p and ORF2p were found to be expressed in rat heart. ORF1p showed a predominantly nuclear localization in cardiomyocytes, whereas ORF2p was exclusively present in endothelial cells. ORF1p levels increased in response to ischemia, which was reversed by antisense ODN treatment. No significant changes in ORF2p were noted. Our results demonstrate that L1 suppression favorably affects postischemic outcome in the heart. Modifying transcriptional activity of L1 may represent a novel anti-ischemic therapeutic strategy.

scholarly journals Retracted: Cardiac release of urocortin precedes the occurrence of irreversible myocardial damage in the rat heart exposed to ischemia/reperfusion injury

FEBS Letters ◽  
2008 ◽  
Vol 582 (6) ◽  
pp. 984-990 ◽  
Author(s):  
Richard A. Knight ◽  
Carol Chen-Scarabelli ◽  
Zhaokan Yuan ◽  
Roy B. McCauley ◽  
J. Di Rezze ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Rat Heart ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Myocardial Damage

Anti-ischemic Effect of German Chamomile (Matricaria recutita L.) Against Ischemia/reperfusion Induced Myocardial Damage in Isolated Rat Heart

Pharmacologia ◽  
2012 ◽  
Vol 3 (9) ◽  
pp. 406-412
Author(s):  
V.M. Chandrashe ◽  
Nirav M. Patel ◽  
R.B. Nidavani ◽  
Jignesh N. Vadiya ◽  
S. Ganapaty
Keyword(s):  
Rat Heart ◽  
Ischemia Reperfusion ◽  
Myocardial Damage ◽  
Isolated Rat Heart ◽  
Matricaria Recutita ◽  
Isolated Rat

Effect of Hydrogen Sulfide on Reactions of Isolated Rat Heart under Volume Load and Ischemia-Reperfusion

2013 ◽  
Vol 4 (3) ◽  
pp. 201-212
Author(s):  
Tetyana V Shimanskaya ◽  
Yulia V. Goshovska ◽  
Olena M. Semenykhina ◽  
Vadim F. Sagach
Keyword(s):  
Hydrogen Sulfide ◽  
Rat Heart ◽  
Ischemia Reperfusion ◽  
Isolated Rat Heart ◽  
Volume Load ◽  
Isolated Rat

Overexpression of miR-431 attenuates hypoxia/reoxygenation-induced myocardial damage via autophagy-related 3

2020 ◽  
Author(s):  
Kang Zhou ◽  
Yan Xu ◽  
Qiong Wang ◽  
Lini Dong
Keyword(s):  
Cell Viability ◽  
Cell Apoptosis ◽  
Myocardial Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Myocardial Damage ◽  
Protective Role ◽  
Human Cardiomyocytes ◽  
Hypoxia Reoxygenation

Abstract Myocardial injury is still a serious condition damaging the public health. Clinically, myocardial injury often leads to cardiac dysfunction and, in severe cases, death. Reperfusion of the ischemic myocardial tissues can minimize acute myocardial infarction (AMI)-induced damage. MicroRNAs are commonly recognized in diverse diseases and are often involved in the development of myocardial ischemia/reperfusion injury. However, the role of miR-431 remains unclear in myocardial injury. In this study, we investigated the underlying mechanisms of miR-431 in the cell apoptosis and autophagy of human cardiomyocytes in hypoxia/reoxygenation (H/R). H/R treatment reduced cell viability, promoted cell apoptotic rate, and down-regulated the expression of miR-431 in human cardiomyocytes. The down-regulation of miR-431 by its inhibitor reduced cell viability and induced cell apoptosis in the human cardiomyocytes. Moreover, miR-431 down-regulated the expression of autophagy-related 3 (ATG3) via targeting the 3ʹ-untranslated region of ATG3. Up-regulated expression of ATG3 by pcDNA3.1-ATG3 reversed the protective role of the overexpression of miR-431 on cell viability and cell apoptosis in H/R-treated human cardiomyocytes. More importantly, H/R treatments promoted autophagy in the human cardiomyocytes, and this effect was greatly alleviated via miR-431-mimic transfection. Our results suggested that miR-431 overexpression attenuated the H/R-induced myocardial damage at least partly through regulating the expression of ATG3.

Abstract 104: Effects of Pinacidil and Ca 2 + on Sodium-loaded Rat Heart Mitochondria

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Sergey M Korotkov ◽  
Vladimir P Nesterov ◽  
Irina V Brailovskaya ◽  
Larisa V Emelyanova ◽  
Svetlana A Konovalova ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Rat Heart ◽  
Mitochondrial Membrane ◽  
Mitochondrial Permeability Transition ◽  
Ischemia Reperfusion ◽  
Potassium Acetate ◽  
Heart Mitochondria ◽  
Inner Mitochondrial Membrane ◽  
Rat Heart Mitochondria ◽  
Acetate Medium

Deterioration of the contractile parameters of the heart muscle caused by ischemia and followed reperfusion is known as the main postoperative complication which is related to Ca 2+ and Na + overload in cardiomyocytes and mitochondria. Pinacidil reduced the overload in ischemia/reperfusion experiments. The mechanism of this phenomenon is still not clear. We hypothesized that increased ion permeability of the inner mitochondrial membrane (IMM) followed drop of electrochemical potential (ΔΨ mito ) can reduce the calcium. The aim of the study was to elucidate the effect of pinacidil (100 μM) and Ca 2+ (100 μM ) on swelling, oxygen consumption and ΔΨ mito of isolated sodium-loaded rat heart mitochondria (RHM(Na)) energized glutamate and malate. Pinacidil significantly enchanced the permeability of IMM to protons in ammonium nitrate medium. Also increased swelling of RHM(Na) energized with substrates in potassium acetate medium revealed that pinacidil increased potassium transport into matrix. Pinacidil stimulated oxygen consumption of RHM(Na) in State 4 and detained Ca 2+ -induced dissipation of ΔΨ mito . Under condition of Ca 2+ and Na + overload simulating ischemia/reperfusion, RHM(Na) oxygen consumption was not affected with pinacidil in State 3 and in the presence of 2,4-dinitrophenol. Cyclosporin A and ADP, the inhibitors of mitochondrial permeability transition pore (MPTP), markedly decreased Ca 2+ - induced swelling of RHM(Na) in nitrate ammonium or potassium acetate medium in the presence of pinacidil. Carboxyatractyloside, an inhibitor of cytosolic side-specific adenine nucleotide translocase, eliminated a pinacidil-stimulated oxygen consumption of succinate-energized RHMNa in State 4 regardless of the presence of Ca 2+ . Pinacidil was also concluded to accelerat potassium flux into energized RHM(Na) and promot MPTP opening in the low conduction state. Based on our data we suggested that the effect of pharmacological preconditioning induced by pinacidil could be due to it’s direct effect on mitochondria which is connected with above stimulation of the potassium permeability of the inner mitochondrial membrane and following reduce of the ΔΨ mito that thus prevent calcium overload of cardiomyocytes after ischemia/reperfusion in turn.

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