Depolarizing-electrode monophasic curves and myocardial infarction ST shift

1962 ◽  
Vol 202 (1) ◽  
pp. 35-40 ◽  
Author(s):  
Gordon E. Dower ◽  
William G. Ziegler ◽  
Margaret A. Geddes ◽  
John A. Osborne
Keyword(s):  
Myocardial Infarction ◽  
Reference Electrode ◽  
Membrane Resistance ◽  
Potassium Ion ◽  
Subtraction Technique ◽  
Cell Interior ◽  
Satisfactory Explanation ◽  
Low Amplitude

The in vivo monophasic curves of the potential variations between an intracellular microelectrode and a remote reference electrode show irregular upstrokes. These can be removed by subtracting from them the ECG recorded from a wire loop surrounding the microelectrode. Since similar irregularities are present in the upstrokes of monophasic curves obtained from potassium-ion depolarizing electrodes, the effect of a similar subtraction technique was tried. Again, sigmoid upstrokes were obtained. The role of the potassium ion is to render the membrane inexcitable at the electrode. The result is that the electrode follows the potential changes of the cell interior with a lag determined by a time constant due to the membrane resistance and the capacitance of the electrode to the rest of the animal. Since the ST changes in myocardial infarction can be considered low amplitude monophasic patterns superimposed on the ECG, and it has been found that the release of potassium from damaged muscle can produce monophasic patterns, it now seems possible to present a satisfactory explanation of such changes.

scholarly journals Garcinoic Acid Improves Cardiac Function and Enhances Angiogenesis Following Myocardial Infarction

2021 ◽  
Author(s):  
Hongyao Hu ◽  
Wei Li ◽  
Yanzhao Wei ◽  
Hui Zhao ◽  
Zhenzhong Wu ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Function ◽  
Ventricular Remodeling ◽  
Vehicle Group ◽  
Potential Mechanism ◽  
Garcinia Kola ◽  
Angiogenic Proteins

Abstract Cardiac ischemia impairs angiogenesis in response to hypoxia, resulting in ventricular remodeling. Garcinoic acid (GA), the extraction from the plant garcinia kola, is validated to attenuate inflammatory response. However, the role of GA in heart failure (HF) and neovascularization after myocardial infarction (MI) is incompletely understood. The present study is striving to explore the role of GA and the potential mechanism of which in cardiac function after MI. SD rats were randomized into sham group, MI+vehicle group, and MI+GA group in vivo. Human umbilical endothelial cells (HUVECs) were cultured in vehicle or GA, and then additionally exposed to 2% hypoxia environment in vitro. MI rats displayed a dramatically reduced myocardial injury, cardiac function and vessel density in the peri-infarcted areas. GA delivery markedly improved cardiac performance and promoted angiogenesis. In addition, GA significantly enhanced tube formation in HUVECs under hypoxia condition. Furthermore, the expressions of pro-angiogenic factors HIF-1α, VEGF-A and bFGF, and pro-angiogenic proteins phospho-VEGFR2Tyr1175 and VEGFR2, as well as phosphorylation levels of Akt and eNOS were increased by GA treatment. In conclusion, GA preserved cardiac function after MI probably via promoting neovascularization. And the potential mechanism may be partially through upregulating the expressions of HIF-1α, VEGF-A, bFGF, phospho-VEGFR2Tyr1175 and VEGFR2 and activating the phosphorylations of Akt and eNOS.

The role of 5-HT7 receptors on isoproterenol-induced myocardial infarction in rats with high-fat diet exacerbated coronary endothelial dysfunction

2020 ◽  
Vol 39 (8) ◽  
pp. 1005-1018 ◽  
Author(s):  
I Cinar ◽  
Z Halici ◽  
B Dincer ◽  
B Sirin ◽  
E Cadirci
Keyword(s):  
Myocardial Infarction ◽  
Endothelial Dysfunction ◽  
High Fat Diet ◽  
Density Lipoprotein ◽  
Heart Tissue ◽  
High Fat ◽  
Inflammatory Status

The presence of 5-HT7r’s in both human and rat cardiovascular and immune tissues and their contribution to inflammatory conditions prompted us to hypothesize that these receptors contribute in acute myocardial infarction (MI) with underlying chronic endothelial dysfunction. We investigated the role of 5-HT7 receptors on heart tissue that damaged by isoproterenol (ISO)-induced MI in rats with high-fat diet (HFD). In vitro and in vivo effects of 5-HT7r agonist (LP44) and antagonist (SB269970) have been investigated on the H9C2 cell line and rats, respectively. For in vivo analyses, rats were fed with HFD for 8 weeks and after this period ISO-induced MI model has been applied to rat. To investigate the role of 5-HT7r’s, two different doses of LP44 and SB269970 were evaluated and compared with standard hypolipidemic agent, atorvastatin. In vitro studies showed that LP44 has protective and proliferative effects on rat cardiomyocytes. Also in in vivo studies stimulating 5-HT7r’s by LP44 improved blood lipid profile (decreased total cholesterol, low-density lipoprotein-C, and triglyceride, increased high-density lipoprotein), decreased cardiac damage markers (creatine kinase and troponin-I), and corrected inflammatory status (tumor necrosis factor-α, interleukin-6). Our results showed significant improvement in LP44 administered rats in terms of histopathologic analyses. In damaged tissues, 5-HT7 mRNA expression increased and agonist administration decreased this elevation significantly. We determined for the first time that 5-HT7r’s are overexpressed in ISO-induced MI of rats with underlying HFD-induced endothelial dysfunction. Restoration of this overexpression by LP44, a 5-HT7r agonist, ameliorated heart tissue in physiopathologic, enzymatic, and molecular level, showing the cardiac role of these receptors and suggesting them as future potential therapeutic targets.

scholarly journals Long Non-Coding RNA 554 Promotes Cardiac Fibrosis via TGF-β1 Pathway in Mice Following Myocardial Infarction

2020 ◽  
Vol 11 ◽  
Author(s):  
Bihui Luo ◽  
Zhiyu He ◽  
Shijun Huang ◽  
Jinping Wang ◽  
Dunzheng Han ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Fibrosis ◽  
Cardiac Fibroblasts ◽  
Non Coding Rna ◽  
Novel Target ◽  
And Function ◽  
Tgf Β1

Rationale: Cardiac fibrosis is observed in nearly every form of myocardial disease. Long non-coding RNAs (lncRNAs) have been shown to play an important role in cardiac fibrosis, but the detailed molecular mechanism remains unknown.Object: We aimed at characterizing lncRNA 554 expression in murine cardiac fibroblasts (CFs) after myocardial infarction (MI) to identify CF-enriched lncRNA and investigate its function and contribution to cardiac fibrosis and function.Methods and Results: In this study, we identified lncRNA NONMMUT022554 (lncRNA 554) as a regulator of MI-induced cardiac fibrosis. We found that lncRNA 554 was significantly up-regulated in the mouse hearts following MI. Further study showed that lncRNA 554 was predominantly expressed in cardiac fibroblasts, indicating a potential role of lncRNA 554 in cardiac fibrosis. In vitro knockdown of lncRNA 554 by siRNA suppressed fibroblasts migration and expression of extracellular matrix (ECM); while overexpression of lncRNA 554 promoted expression of ECM genes. Consistently, lentivirus mediated in vivo knockdown of lncRNA 554 could inhibit cardiac fibrosis and improve cardiac function in mouse model of MI. More importantly, TGF-β1 inhibitor (TEW-7197) could reverse the pro-fibrotic function of lncRNA 554 in CFs. This suggests that the effects of lncRNA 554 on cardiac fibrosis is TGF-β1 dependent.Conclusion: Collectively, our study illustrated the role of lncRNA 554 in cardiac fibrosis, suggested that lncRNA 554 might be a novel target for cardiac fibrosis.

scholarly journals Exosomes Secreted from CXCR4 Overexpressing Mesenchymal Stem Cells Promote Cardioprotection via Akt Signaling Pathway following Myocardial Infarction

2015 ◽  
Vol 2015 ◽  
pp. 1-14 ◽  
Author(s):  
Kai Kang ◽  
Ruilian Ma ◽  
Wenfeng Cai ◽  
Wei Huang ◽  
Christian Paul ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Infarct Size ◽  
Functional Restoration ◽  
Akt Inhibitor ◽  
Cardiac Functions

Background and Objective.Exosomes secreted from mesenchymal stem cells (MSC) have demonstrated cardioprotective effects. This study examined the role of exosomes derived from MSC overexpressing CXCR4 for recovery of cardiac functions after myocardial infarction (MI).Methods. In vitro, exosomes from MSC transduced with lentiviral CXCR4 (ExoCR4) encoding a silencing sequence or null vector were isolated and characterized by transmission electron microscopy and dynamic light scattering. Gene expression was then analyzed by qPCR and Western blotting. Cytoprotective effects on cardiomyocytes were evaluated and effects of exosomes on angiogenesis analyzed.In vivo, an exosome-pretreated MSC-sheet was implanted into a region of scarred myocardium in a rat MI model. Angiogenesis, infarct size, and cardiac functions were then analyzed.Results. In vitro, ExoCR4significantly upregulatedIGF-1αand pAkt levels and downregulated active caspase 3 levelin cardiomyocytes. ExoCR4also enhanced VEGF expression and vessel formation. However, effects of ExoCR4were abolished by an Akt inhibitor or CXCR4 knockdown.In vivo, ExoCR4treated MSC-sheet implantation promoted cardiac functional restoration by increasing angiogenesis, reducing infarct size, and improving cardiac remodeling.Conclusions.This study reveals a novel role of exosomes derived from MSCCR4and highlights a new mechanism of intercellular mediation of stem cells for MI treatment.

scholarly journals Histidine triad nucleotide-binding protein 2 protects cardiomyocytes via maintaining NAD homeostasis in virto and in vivo

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
F Mengkang ◽  
Y.I.N Huang ◽  
J Qian
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Molecular Docking ◽  
Nucleotide Binding ◽  
Metabolic Status ◽  
Funding Source ◽  
Targeted Metabolomics ◽  
Pet Ct

Abstract Background Heart failure (HF) is the end-stage of most heart diseases with poor clinical outcomes. The mitochondrial dysfunction is a critical therapeutic target in HF, and the histidine triad nucleotide-binding (HINT2) protein has been shown to enhance energy metabolism in liver. However, the role of HINT2 in HF remains unclear. Purpose To explore the role of the histidine triad nucleotide-binding 2 (HINT2) protein in heart failure. Methods Neonatal mouse ventricle myocytes (NMVMs) and myocardial infarction-induced heart failure mice were used for in vitro or in vivo experiments. Adenovirus (ADV) and adeno-associated virus serum type 9 (AAV9) vectors were used to regulate HINT2 expression. The expression of HINT2 was determined by quantifying the mRNA and protein levels. Cell survival was analysed using the CCK-8 kit and TUNEL staining. Mitochondrial function was determined by the mitochondrial membrane potential and oxygen consumption rates. AAV9-HINT2 was injected 24 h post myocardial infarction following which transthoracic echocardiography and histological analyses were performed after 4 weeks. Positron emission tomography tomography-computed tomography (PET/CT) and targeted metabolomics analyses were used to explore the metabolic status in vivo. NAD levels were measured using a colorimetric kit. Computer-simulated rigid body molecular docking was performed using AUTODOCK4. Molecule binding kinetics assays were performed using biolayer interferometry. Results After 12 hours hypoxia stimuli, HINT2 was down regulated. ADV-HINT2 induced HINT2 overexpression improved NMVMs survival and reduced apoptosis after hypoxia. MMP was reduced in ADV-shHINT2 group and was preserved in ADV-HINT2 group under hypoxia. HINT2 overexpressed NMVMs showed less reduction in basal, ATP-linked and maximum OCR after hypoxia stimuli. In vivo experiment, showed that cardiac function and metabolic status was preserved by HINT2 overexpression. PET/CT displayed glucose uptake ability was significantly reduced in in failing heart, which was preserved by overexpression of HINT2. Targeted metabolomics analysis showed that nicotinate and nicotinamide metabolism pathway was regulated by HINT2, in which oxidized state NAD (NAD+) and redox state NAD (NADH) was increased in AAV9-HINT2 group. NAD concentration was detected in NMVMs. HINT2 can improve total NAD level rather than ratio of NAD+/NADH, and its effect was limited into mitochondria.HINT2 overexpression restored mitochondrial NAD levels; this was dependent on nicotinamide mononucleotide (NMN). Using computer-simulated molecular docking analysis and biolayer interferometry, we observed that HINT2 potentially binds and associates with NMN. Conclusion In summary, these findings demonstrate that the HINT2 is beneficial to preserve the heart function and metabolism in the HF murine model after acute MI, and this positive effect may due to the maintenance of mitochondrial NAD homeostasis. Funding Acknowledgement Type of funding source: Foundation. Main funding source(s): National Natural Science Foundation of China (Grant Nos: 81970295, 81870267)

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