scholarly journals The mechanism of action of metabolic cytoprotector trimetazidine in acute ischemia-reperfusion injury

2014 ◽  
Vol 5 (2) ◽  
pp. 24-30
Author(s):  
M. G Glezer ◽  
E. I Astashkin ◽  
M. V Novikova
Keyword(s):  
Reperfusion Injury ◽  
Mechanism Of Action ◽  
Stress Reduction ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Myocardial Damage ◽  
Acute Ischemia ◽  
Positive Effects ◽  
Coronary Syndrome ◽  
New Concepts

The review presents, as the classical data on the mechanism of action of metabolic cytoprotector trimetazidine in acute ischemia/reperfusion injury associated with a partial inhibition of the oxidation of long chain fatty acids and increased metabolism of pyruvate, as well as new concepts of reducing the level of oxidative stress, reduction of cardiomyocyte apoptosis, elimination areas of myocardial stunning and hibernation state. Described cytoprotective effects associated with inhibition of activation of mitochondrial pore with transient (temporary) permeability. Presented clinical studies showing significant anti-anginal and anti-ischemic effect of the trimetazidine in patients with stable angina, to decrease myocardial damage in acute coronary syndrome, during intervention on the coronary arteries. Particular attention is given to the latest data on the positive effects of prolonged use of trimetazidine on the course and prognosis in patients with heart failure.

IKKβ inhibition attenuates myocardial injury and dysfunction following acute ischemia-reperfusion injury

2007 ◽  
Vol 293 (4) ◽  
pp. H2248-H2253 ◽  
Author(s):  
Nancy C. Moss ◽  
William E. Stansfield ◽  
Monte S. Willis ◽  
Ru-Hang Tang ◽  
Craig H. Selzman
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Cardiac Injury ◽  
Myocardial Damage ◽  
Nuclear Factor Κb ◽  
Left Ventricular ◽  
Acute Ischemia ◽  
Artery Ligation ◽  
Cardiac Morbidity

Despite years of experimental and clinical research, myocardial ischemia-reperfusion (IR) remains an important cause of cardiac morbidity and mortality. The transcription factor nuclear factor-κB (NF-κB) has been implicated as a key mediator of reperfusion injury. Activation of NF-κB is dependent upon the phosphorylation of its inhibitor, IκBα, by the specific inhibitory κB kinase (IKK) subunit, IKKβ. We hypothesized that specific antagonism of the NF-κB inflammatory pathway through IKKβ inhibition reduces acute myocardial damage following IR injury. C57BL/6 mice underwent left anterior descending (LAD) artery ligation and release in an experimental model of acute IR. Bay 65-1942, an ATP-competitive inhibitor that selectively targets IKKβ kinase activity, was administered intraperitoneally either prior to ischemia, at reperfusion, or 2 h after reperfusion. Compared with untreated animals, mice treated with IKKβ inhibition had significant reduction in left ventricular infarct size. Cardiac function was also preserved following pretreatment with IKKβ inhibition. These findings were further associated with decreased expression of phosphorylated IκBα and phosphorylated p65 in myocardial tissue. In addition, IKKβ inhibition decreased serum levels of TNF-α and IL-6, two prototypical downstream effectors of NF-κB activity. These results demonstrate that specific IKKβ inhibition can provide both acute and delayed cardioprotection and offers a clinically accessible target for preventing cardiac injury following IR.

scholarly journals Cardioprotective mechanism of FTY720 in ischemia reperfusion injury

2019 ◽  
Vol 30 (5) ◽  
Author(s):  
Naseer Ahmed
Keyword(s):  
Heart Failure ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Myocardial Damage ◽  
New Drugs ◽  
Mortality And Morbidity ◽  
Coronary Syndrome

Abstract Cardioprotection is a very challenging area in the field of cardiovascular sciences. Myocardial damage accounts for nearly 50% of injury due to reperfusion, yet there is no effective strategy to prevent this to reduce the burden of heart failure. During last couple of decades, by combining genetic and bimolecular studies, many new drugs have been developed to treat hypertension, heart failure, and cancer. The use of percutaneous coronary intervention has reduced the mortality and morbidity of acute coronary syndrome dramatically. However, there is no standard therapy available that can mitigate cardiac reperfusion injury, which contributes to up to half of myocardial infarcts. Literature shows that the activation of sphingosine receptors, which are G protein-coupled receptors, induces cardioprotection both in vitro and in vivo. The exact mechanism of this protection is not clear yet. In this review, we discuss the mechanism of ischemia reperfusion injury and the role of the FDA-approved sphingosine 1 phosphate drug fingolimod in cardioprotection.

scholarly journals Extracellular vesicles from patients with Acute Coronary Syndrome impact on ischemia-reperfusion injury

2021 ◽  
pp. 105715
Author(s):  
Fabrizio D’Ascenzo ◽  
Saveria Femminò ◽  
Francesco Ravera ◽  
Filippo Angelini ◽  
Andrea Caccioppo ◽  
...  
Keyword(s):  
Acute Coronary Syndrome ◽  
Reperfusion Injury ◽  
Extracellular Vesicles ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Coronary Syndrome

scholarly journals Dexamethasone Protects Against Tourniquet-Induced Acute Ischemia-Reperfusion Injury in Mouse Hindlimb

2018 ◽  
Vol 9 ◽  
Author(s):  
Ryan M. Corrick ◽  
Huiyin Tu ◽  
Dongze Zhang ◽  
Aaron N. Barksdale ◽  
Robert L. Muelleman ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Acute Ischemia

Myocardial ischemia-reperfusion injury is enhanced in a model of systemic allergy and asthma

2004 ◽  
Vol 286 (5) ◽  
pp. H1720-H1725 ◽  
Author(s):  
Surovi Hazarika ◽  
Michael R. Van Scott ◽  
Robert M. Lust
Keyword(s):  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Neutrophil Infiltration ◽  
Acute Ischemia ◽  
Strong Positive Correlation ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion ◽  
Allergy And Asthma

Despite epidemiological evidence of cardiovascular complications in asthmatics, the direct contribution of asthmatic pathophysiology to cardiovascular effects is unknown. Considering parallels in underlying pathophysiology, we tested the hypothesis that presence of systemic allergy and asthma worsens the outcome of myocardial ischemia-reperfusion injury. Systemic allergy and asthma were created in rabbits by repeated intraperitoneal injections of allergen with adjuvant, followed by an airway challenge in two groups. Nonsensitized animals served as controls. In situ myocardial ischemia-reperfusion was induced in anesthetized animals by a 30-min ligation of a coronary artery, followed by 3 h of reperfusion. Ischemia-reperfusion was done at 24 h after intraperitoneal boost (1 DB) and 7 days (7 DB) after the last intraperitoneal injection and at 24 h (1DAWCH) and 7 days (7DAWCH) after airway challenge. The infarct size (determined by 2,3,5-triphenyltetrazolium chloride staining, normalized to area at risk) was significantly higher in all sensitized groups compared with control (1DB, 31 ± 4; 7DB, 28.9 ± 2.6; 1DAWCH, 66.1 ± 4.1; 7DAWCH, 28.9 ± 9.2; control, 16.7 ± 3.2; means ± SE; P < 0.01 by ANOVA; n = 6). The 1DAWCH group showed significantly greater infarct than all other groups ( P < 0.05). Myocardial neutrophil infiltration was significantly higher in the sensitized groups compared with control ( P < 0.01). Tissue neutrophil counts showed a strong positive correlation to infarct sizes ( r2 = 0.9). These observations indicate that the presence of systemic allergy and asthma is associated with increased myocardial neutrophil infiltration during acute ischemia-reperfusion and increased size of the resulting infarct.

scholarly journals Cardiac progenitor-derived exosomes protect ischemic myocardium from acute ischemia/reperfusion injury

2013 ◽  
Vol 431 (3) ◽  
pp. 566-571 ◽  
Author(s):  
Lijuan Chen ◽  
Yingjie Wang ◽  
Yaohua Pan ◽  
Lan Zhang ◽  
Chengxing Shen ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Ischemic Myocardium ◽  
Acute Ischemia
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