Resveratrol Protects Left Ventricle by Increasing Adenylate Kinase 1 and Isocitrate Dehydrogenase Activities in Rats with Myocardial Infarction

2012 ◽  
Keyword(s):  
Myocardial Infarction ◽  
Left Ventricle ◽  
Isocitrate Dehydrogenase ◽  
Adenylate Kinase ◽  
Adenylate Kinase 1

scholarly journals The Use of Artificial Hypoxia in Endurance Training in Patients after Myocardial Infarction

2021 ◽  
Vol 18 (4) ◽  
pp. 1633 ◽  
Author(s):  
Agata Nowak-Lis ◽  
Tomasz Gabryś ◽  
Zbigniew Nowak ◽  
Paweł Jastrzębski ◽  
Urszula Szmatlan-Gabryś ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Left Ventricle ◽  
Endurance Training ◽  
Exercise Tolerance ◽  
Collateral Circulation ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Test Duration ◽  
Hemodynamic Parameters ◽  
Ventricular Ejection Fraction

The presence of a well-developed collateral circulation in the area of the artery responsible for the infarction improves the prognosis of patients and leads to a smaller area of infarction. One of the factors influencing the formation of collateral circulation is hypoxia, which induces angiogenesis and arteriogenesis, which in turn cause the formation of new vessels. The aim of this study was to assess the effect of endurance training conducted under normobaric hypoxia in patients after myocardial infarction at the level of exercise tolerance and hemodynamic parameters of the left ventricle. Thirty-five patients aged 43–74 (60.48 ± 4.36) years who underwent angioplasty with stent implantation were examined. The program included 21 training units lasting about 90 min. A statistically significant improvement in exercise tolerance assessed with the cardiopulmonary exercise test (CPET) was observed: test duration (p < 0.001), distance covered (p < 0.001), HRmax (p = 0.039), maximal systolic blood pressure (SBPmax) (p = 0.044), peak minute ventilation (VE) (p = 0.004) and breathing frequency (BF) (p = 0.044). Favorable changes in left ventricular hemodynamic parameters were found for left ventricular end-diastolic dimension LVEDD (p = 0.002), left ventricular end-systolic dimension LVESD (p = 0.015), left ventricular ejection fraction (LVEF) (p = 0.021), lateral e’ (p < 0.001), septal e’ (p = 0.001), and E/A (p = 0.047). Endurance training conducted in hypoxic conditions has a positive effect on exercise tolerance and the hemodynamic indicators of the left ventricle.

Injection of a novel synthetic hydrogel preserves left ventricle function after myocardial infarction

2009 ◽  
Vol 90A (2) ◽  
pp. 472-477 ◽  
Author(s):  
Xue-Jun Jiang ◽  
Tao Wang ◽  
Xiao-Yan Li ◽  
De-Qun Wu ◽  
Zhao-Bin Zheng ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Left Ventricle ◽  
Left Ventricle Function ◽  
Synthetic Hydrogel ◽  
Ventricle Function

Immunization with recombinant schistosome adenylate kinase 1 partially protects mice against Schistosoma japonicum infection

2017 ◽  
Vol 116 (6) ◽  
pp. 1665-1674 ◽  
Author(s):  
Yanru Gao ◽  
Xiaoshan Zhou ◽  
Huan Wang ◽  
Rong Liu ◽  
Qing Ye ◽  
...  
Keyword(s):  
Schistosoma Japonicum ◽  
Adenylate Kinase ◽  
Adenylate Kinase 1

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.

Abstract 58: AT2 Receptor Agonism Regulates TIMP1/MMP9 Axis in the Heart Preventing Cardiac Fibrosis and Improving Heart Function After Experimental Myocardial Infarction

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Dilyara Lauer ◽  
Svetlana Slavic ◽  
Manuela Sommerfeld ◽  
Christa Thöne-Reineke ◽  
Yuliya Sharkovska ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Left Ventricle ◽  
Late Stage ◽  
Heart Function ◽  
Cardiac Fibroblasts ◽  
Collagen Content ◽  
Vehicle Group ◽  
At2 Receptor ◽  
Down Regulation ◽  
Tgf Β1

Aims: A selective nonpeptide agonist for the angiotensin AT2 receptor compound 21 (C21) improved cardiac functions 7 days after myocardial infarction (MI). Here, we aimed to investigate what are the cellular mechanisms underlying cardiac protection in the late stage after MI. Methods and Results: MI was induced in Wistar rats by permanent ligation of the left coronary artery. Treatment with C21 (0.03mg/kg i.p. daily) started 6h after MI and continued for 6 weeks. Hemodynamic parameters were measured via transthoracic Doppler echocardiography and intracardiac Samba catheter. The expression of MMP9, TIMP1, TGF-β1 and collagen content were determined in left ventricle. Anti-proteolytic effects were additionally studied in primary cardiac fibroblasts. C21 significantly improved systolic and diastolic function 6 weeks after MI in comparison with the vehicle group as shown by ejection fraction (71.2±4.7 % vs. 53.4±7.0%; p<0.001), fractional shortening (40.8±2.3% vs. 30.9±3.1%; p<0.05), LVIDs (4.4±0.5mm vs. 5.2±0.8mm; p<0.05), LV EDP (16.9±1.2mmHg vs. 22.1±1.4mmHg; p<0.05), E/A ratio, dP/dt max and dP/dt min (p<0.05). Moreover, C21 improved arterial stiffness parameter (AIx) (18±1.2% vs. 25%±1.8, p<0.05) and reduced collagen content (15%; p<0.05) in postinfarcted myocardium. TIMP1 protein expression in the left ventricle was strongly up-regulated (17.7-fold; p<0.05) whereas MMP9 and TGF-β1 were significantly down-regulated (1.5-fold, p<0.05; 3.4-fold p<0.001, respectively) in the treated group. In cardiac fibroblasts, C21 primarily induced TIMP1 expression followed by attenuated MMP9 secretion and TGF-β1 down-regulation. Conclusion: C21 improves heart function in the late stage after MI and prevents cardiac remodeling. Activation of TIMP1 and subsequent inhibition of MMP9-mediated proteolysis as well as down-regulation of TGF-β1 followed by decreased collagen accumulation may attenuate disintegration of the extracellular matrix and reduce fibrosis.

ANEURYSM OF THE LEFT VENTRICLE SECONDARY TO MYOCARDIAL INFARCTION

1949 ◽  
Vol 42 (4) ◽  
pp. 323-325
Author(s):  
H L Newbold ◽  
G B Wyatt ◽  
T F Frist
Keyword(s):  
Myocardial Infarction ◽  
Left Ventricle

scholarly journals S100A9 is a functional effector of infarct wall thinning after myocardial infarction

2021 ◽  
Author(s):  
Upendra Chalise ◽  
Mediha Becirovic-Agic ◽  
Michael J Daseke II ◽  
Shelby R. Konfrst ◽  
Jocelyn R. Rodriguez-Paar ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Left Ventricle ◽  
Neutrophil Infiltration ◽  
Vehicle Control ◽  
Macrophage Infiltration ◽  
Secreted Protein ◽  
Cardiac Physiology ◽  
Wall Thinning ◽  
Saline Vehicle ◽  
Lower Ejection Fraction

Neutrophils infiltrate into the left ventricle (LV) early after myocardial infarction (MI) and launch a pro-inflammatory response. Along with neutrophil infiltration, LV wall thinning due to cardiomyocyte necrosis also peaks at day 1 in the mouse model of MI. To understand the correlation, we examined a previously published dataset that included day 0 (n=10) and MI day 1 (n=10) neutrophil proteome and echocardiography assessments. Out of 123 proteins, 4 proteins positively correlated with the infarct wall thinning index (1/wall thickness): histone 1.2 (r=0.62, p=0.004), S100A9 (r=0.60, p=0.005), histone 3.1 (r=0.55, p=0.01), and fibrinogen (r=0.47, p=0.04). As S100A9 was the highest ranked secreted protein, we hypothesized that S100A9 is a functional effector of infarct wall thinning. We exogenously administered S100A8/A9 at the time of MI to mice (C57BL/6J, male, 3-6 months of age, n=7M (D1), and n=5M (D3)) and compared to saline vehicle control treated mice (n=6M (D1) and n=6M (D3)) at MI days 1 and 3. At MI day 3, the S100A8/A9 group showed a 22% increase in the wall thinning index compared to saline (p=0.02), along with higher dilation and lower ejection fraction. The decline in cardiac physiology occurred subsequent to increased neutrophil and macrophage infiltration at MI day 1 and increased macrophage infiltration at D3. Our results reveal that S100A9 is a functional effector of infarct wall thinning.

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