Effects of In Vivo Administration of an Endothelial KCa Channel Activator on Recovery of Cardiac Function Following Acute Myocardial Infarction in Mice

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Tae yeob Kim ◽  
Darrell D. Belke ◽  
Ramesh C. Mishra ◽  
Andrew P. Braun
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Cardiac Function ◽  
In Vivo Administration ◽  
Channel Activator

scholarly journals Co-transplantation of Hypoxia Pretreated Human Adipose Derived Mesenchymal Stem Cells and Cord Blood Mononuclear Cells to Treat Rats with Acute Myocardial Infarction

2020 ◽  
Author(s):  
Hang Xiang ◽  
Tianyuan Xiang ◽  
Hongxia Zhang ◽  
Ann Xu ◽  
Matthew John Horwedel ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Stem Cells ◽  
Cardiac Function ◽  
Mononuclear Cells ◽  
The Other ◽  
In Vivo Studies ◽  
Blood Mononuclear Cells ◽  
Cord Blood Mononuclear Cells

Abstract BackgroundHuman adipose derived mesenchymal stem cells (ASCs) are ideal candidates for the treatment of acute myocardial infarction (AMI), due to their favorable availability and regenerative potential. However, in vivo studies showed that ASCs are not resilient at the infarcted area, for a shortage of blood and oxygen supply. Hypoxic pretreatment was proven to be an effective way to enhance cell survival in ischemic atmosphere. Moreover, co-transplantation of stem cells was another promising strategy to improve cardiac function after transplantation. So, we hypothesized that hypoxic pretreated ASCs combined with proangiogenic cord blood mononuclear cells (CBMNCs) would promote treatment efficacy after co-transplantation.MethodsASCs extracted from male volunteer were preconditioned in hypoxic condition (HP-ASC) for 24h, and total RNA were extracted after that. Gene expressions were compared between HP-ASC and ASC. Then, we transplanted stem cells to female Wistar rats which divided into different groups: (1) HP-ASCs group (n=10, 1x106ASCs); (2) HP-ASCs + CBMNCs group (n=10, 0.5×106 ASCs+0.5×106 CBMNCs); (3) CBMNCs group (n=10, 1×106 ASCs); (4) Control group (n=10, 40μL PBS); (5) Sham group (n=10). Echocardiogram was performed before (0d) and after (30d) after cell transplantation. Hearts were harvested at 30d to analyze the infarct size, myocardium apoptosis, stem cells viability and angiogenesis. ResultsIn vitro study showed that HP-ASCs had a wide range of paracrine function, with the incretion growth factors and their receptors, which would support the cell survivals. In addition, HP-ASCs also gained potentials in hypoxic adaptation (increased expression of HO-1 and SDF-1), as well as homing and immigrating abilities (CXCR4, ICAM-1 and ICAM-2). In vivo studies showed that, 30 days after transplantation in AMI rats, the HP-ASCs group had a better improvement in cardiac function; reduction of the infarct size; and decrease of ASCs death than the other groups (HP-ASCs > HP-ASCs + CBMNCs ≧ CBMNCs > PBS) (p<0.05). However, the combined group of HP-ASCs and CBMNCs had more significant angiogenesis than the other groups (HP-ASCs + CBMNCs > CBMNCs > HP-ASCs > PBS) (p <0.05).ConclusionsHP-ASCs alone had a greater potential in improving cardiac function in AMI rats. However, the combination of HP-ASCs and CBMNCs had a better result in angiogenesis.

scholarly journals Continuous Infusion of Angiotensin IV Protects against Acute Myocardial Infarction via the Inhibition of Inflammation and Autophagy

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Wen-wu Bai ◽  
Hao Wang ◽  
Chun-hua Gao ◽  
Ke-yin Liu ◽  
Bing-xiu Guo ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Cardiac Function ◽  
Cardiomyocyte Apoptosis ◽  
Neonatal Rat ◽  
Infarction Size ◽  
Hypoxia Group ◽  
Ang Iv

Acute myocardial infarction (AMI) is a major cause of morbidity and mortality worldwide. Angiotensin (Ang) IV possesses many biological properties that are not yet completely understood. Therefore, we investigated the function and mechanism of Ang IV in AMI in in vivo and in vitro conditions. AMI was performed by ligation of the left anterior descending coronary artery (LAD) in male C57 mice. Ang IV was continuously infused by a minipump 3 d before AMI for 33 d. The neonatal rat ventricular myocytes (NRVCs) were stimulated with Ang IV and cultured under hypoxic conditions. In vivo, Ang IV infusion significantly reduced the mortality after AMI. By the 7th day after AMI, compared with the AMI group, Ang IV reduced the inflammatory cytokine expression. Moreover, terminal deoxyribonucleotidyl transferase- (TDT-) mediated dUTP nick-end labeling (TUNEL) assay showed that Ang IV infusion reduced AMI-induced cardiomyocyte apoptosis. Compared with AMI, Ang IV reduced autophagosomes in cardiomyocytes and improved mitochondrial swelling and disarrangement, as assessed by transmission electron microscopy. By 30th day after AMI, Ang IV significantly reduced the ratio of heart weight to body weight. Echocardiography showed that Ang IV improved impaired cardiac function. Hematoxylin and eosin (H&E) and Masson staining showed that Ang IV infusion reduced the infarction size and myocardial fibrosis. In vitro, dihydroethidium (DHE) staining and comet assay showed that, compared with the hypoxia group, Ang IV reduced oxidative stress and DNA damage. Enzyme-linked immunosorbent assay (ELISA) showed that Ang IV reduced hypoxia-induced secretion of the tumor necrosis factor- (TNF-) ɑ and interleukin- (IL-) 1β. In addition, compared with the hypoxia group, Ang IV reduced the transformation of light chain 3- (LC3-) I to LC3-II but increased p62 expression and decreased cardiomyocyte apoptosis. Overall, the present study showed that Ang IV reduced the inflammatory response, autophagy, and fibrosis after AMI, leading to reduced infarction size and improved cardiac function. Therefore, administration of Ang IV may be a feasible strategy for the treatment of AMI.

scholarly journals Author Correction: In vivo transduction of ETV2 improves cardiac function and induces vascular regeneration following myocardial infarction

2019 ◽  
Vol 51 (9) ◽  
pp. 1-1 ◽  
Author(s):  
Sunghun Lee ◽  
Dong Hun Lee ◽  
Bong-Woo Park ◽  
Ri Youn Kim ◽  
Anh Duc Hoang ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Function ◽  
Vascular Regeneration

Stabilization of hypoxia inducible factor rather than modulation of collagen metabolism improves cardiac function after acute myocardial infarction in rats

2006 ◽  
Vol 8 (4) ◽  
pp. 347-354 ◽  
Author(s):  
Sebastian Philipp ◽  
Jan Steffen Jürgensen ◽  
Jens Fielitz ◽  
Wanja M. Bernhardt ◽  
Alexander Weidemann ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Cardiac Function ◽  
Hypoxia Inducible Factor ◽  
Collagen Metabolism

scholarly journals Galectin-3 and Cardiac Function in Survivors of Acute Myocardial Infarction

2013 ◽  
Vol 6 (3) ◽  
pp. 492-498 ◽  
Author(s):  
Robin A.P. Weir ◽  
Colin J. Petrie ◽  
C. Aengus Murphy ◽  
Suzanne Clements ◽  
Tracey Steedman ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Cardiac Function ◽  
Galectin 3

Abstract 12: EMMPRIN-Targeted Magnetic Nanoparticles for in vivo Visualization and Regression of Acute Myocardial Infarction in a Model of Acute Coronary Artery Occlusion

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Irene Cuadrado ◽  
Maria Jose Garcia Miguel ◽  
Irene Herruzo ◽  
Mari Carmen Turpin ◽  
Ana Martin ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Extracellular Matrix ◽  
Coronary Artery ◽  
Left Ventricle ◽  
Infarct Size ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Gadolinium Enhancement

Extracellular matrix metalloproteinase inducer EMMPRIN, is highly expressed in patients with acute myocardial infarction (AMI), and induces activation of several matrix metalloproteinases (MMPs), including MMP-9 and MMP-13. To prevent Extracellular matrix degradation and cardiac cell death we targeted EMMPRIN with paramagnetic/fluorescent micellar nanoparticles with an EMMPRIN binding peptide AP9 conjugated (NAP9), or an AP9 scramble peptide as a negative control (NAPSC). NAP9 binds to endogenous EMMPRIN as detected by confocal microscopy of cardiac myocytes and macrophages incubated with NAP and NAPSC in vitro, and in vivo in mouse hearts subjected to left anterior descending coronary artery occlusion (IV injection 50mγ/Kg NAP9 or NAP9SC). Administration of NAP9 at the same time or 1 hour after AMI reduced infarct size over a 20% respect to untreated and NAPSC injected mice, recovered left ventricle ejection fraction (LVEF) similar to healthy controls, and reduced EMMPRIN downstream MMP9 expression. In magnetic resonance scans of mouse hearts 2 days after AMI and injected with NAP9, we detected a significant gadolinium enhancement in the left ventricle respect to non-injected mice and to mice injected with NAPSC. Late gadolinium enhancement assays exhibited NAP9-mediated left ventricle signal enhancement as early as 30 minutes after nanoprobe injection, in which a close correlation between the MRI signal enhancement and left ventricle infarct size was detected. Taken together, these results point EMMPRIN targeted nanoprobes as a new tool for the treatment of AMI.

scholarly journals Correlation of Triiodothyronine Level with In-Hospital Cardiac Function and Long-Term Prognosis in Patients with Acute Myocardial Infarction

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Jianqing She ◽  
Jiahao Feng ◽  
Yangyang Deng ◽  
Lizhe Sun ◽  
Yue Wu ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Survival Analysis ◽  
Cardiac Function ◽  
Thyroid Function ◽  
Major Adverse Cardiovascular Events ◽  
Free Triiodothyronine ◽  
Kaplan Meier ◽  
Significant Difference

Objective. The pathophysiologic mechanism of how thyroid function is related to the development and prognosis of acute myocardial infarction (AMI) remains under explored, and there has been a lack of clinical investigations. In this study, we investigate the relationship between triiodothyronine (T3) level and cardiac ejection fraction (EF) as well as probrain natriuretic peptide (NT-proBNP) on admission and subsequent prognosis in AMI patients. Methods. We measured admission thyroid function, NT-proBNP, and EF by echocardiography in 345 patients diagnosed with AMI. Simple and multiregression analyses were performed to investigate the correlation between T3 level and EF as well as NT-proBNP. Major adverse cardiovascular events (MACE), including new-onset myocardial infarction, acute heart failure, and cardiac death, were documented during the follow-up. 248 participants were separated into three groups based on T3 and free triiodothyronine (FT3) levels for survival analysis during a 2-year follow-up. Results. 345 patients diagnosed with AMI were included in the initial observational analysis. 248 AMI patients were included in the follow-up survival analysis. The T3 levels were found to be significantly positively correlated with EF (R square=0.042, P<0.001) and negatively correlated with admission NT-proBNP levels (R square=0.059, P<0.001), which is the same with the correlation between FT3 and EF (R square=0.053, P<0.001) and admission NT-proBNP levels (R square=0.108, P<0.001). Kaplan-Meier survival analysis revealed no significant difference with regard to different T3 or FT3 levels at the end of follow-up. Conclusions. T3 and FT3 levels are moderately positively correlated with cardiac function on admission in AMI patients but did not predict a long-time survival rate. Further studies are needed to explain whether longer-term follow-up would further identify the prognosis effect of T3 on MACE and all-cause mortality.

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