scholarly journals Use of Multifactorial Treatments to Address the Challenge of Translating Experimental Myocardial Infarct Reduction Strategies

2019 ◽  
Vol 20 (6) ◽  
pp. 1449 ◽  
Author(s):  
Julie Horton ◽  
Jitka Virag
Keyword(s):  
Cardiac Muscle ◽  
Tissue Damage ◽  
Molecular Basis ◽  
Myocardial Injury ◽  
Myocardial Infarct ◽  
Myocardial Tissue ◽  
Ischemic Event ◽  
Reduction Strategies ◽  
Candidate Molecule ◽  
Experimental Myocardial Infarct

Myocardial tissue damage that occurs during an ischemic event leads to a spiraling deterioration of cardiac muscle structural and functional integrity. Reperfusion is the only known efficacious strategy and is the most commonly used treatment to reduce injury and prevent remodeling. However, timing is critical, and the procedure is not always feasible for a variety of reasons. The complex molecular basis for cardioprotection has been studied for decades but formulation of a viable therapeutic that can significantly attenuate myocardial injury remains elusive. In this review, we address barriers to the development of a fruitful approach that will substantially improve the prognosis of those suffering from this widespread and largely unmitigated disease. Furthermore, we proffer that ephrinA1, a candidate molecule that satisfies many of the important criteria discussed, possesses robust potential to overcome these hurdles and thus offers protection that surpasses the limitations currently observed.

scholarly journals Molecular Basis of Cardioprotective Effect of Antioxidant Vitamins in Myocardial Infarction

2013 ◽  
Vol 2013 ◽  
pp. 1-15 ◽  
Author(s):  
Ramón Rodrigo ◽  
Matías Libuy ◽  
Felipe Feliú ◽  
Daniel Hasson
Keyword(s):  
Myocardial Infarction ◽  
Reperfusion Injury ◽  
Tissue Damage ◽  
Molecular Basis ◽  
Ischemia Reperfusion Injury ◽  
Myocardial Infarct ◽  
Ischemia Reperfusion ◽  
Antioxidant Vitamins ◽  
Cardioprotective Effect ◽  
Percutaneous Coronary Angioplasty

Acute myocardial infarction (AMI) is the leading cause of mortality worldwide. Major advances in the treatment of acute coronary syndromes and myocardial infarction, using cardiologic interventions, such as thrombolysis or percutaneous coronary angioplasty (PCA) have improved the clinical outcome of patients. Nevertheless, as a consequence of these procedures, the ischemic zone is reperfused, giving rise to a lethal reperfusion event accompanied by increased production of reactive oxygen species (oxidative stress). These reactive species attack biomolecules such as lipids, DNA, and proteins enhancing the previously established tissue damage, as well as triggering cell death pathways. Studies on animal models of AMI suggest that lethal reperfusion accounts for up to 50% of the final size of a myocardial infarct, a part of the damage likely to be prevented. Although a number of strategies have been aimed at to ameliorate lethal reperfusion injury, up to date the beneficial effects in clinical settings have been disappointing. The use of antioxidant vitamins could be a suitable strategy with this purpose. In this review, we propose a systematic approach to the molecular basis of the cardioprotective effect of antioxidant vitamins in myocardial ischemia-reperfusion injury that could offer a novel therapeutic opportunity against this oxidative tissue damage.

scholarly journals Therapeutic activity of sarpogrelate and dopamine D2 receptor agonists on cardiovascular and renal systems in rats with alloxan-induced diabetes

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Mohammed Ahmed Fouad Shalaby ◽  
Hekma A. Abd El Latif ◽  
Mohamed El Yamani ◽  
May Ahmed Galal ◽  
Sherifa Kamal ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Myocardial Injury ◽  
Troponin I ◽  
Staining Method ◽  
Myocardial Infarct ◽  
Myocardial Infarct Size ◽  
Blood Concentrations ◽  
Receptor Agonists ◽  
Long Term Treatment ◽  
Kidney Hypertrophy

Abstract Background Dopamine D2 receptor agonists, bromocriptine and cabergoline, are notable medications in the treatment of Parkinsonism, hyperprolactinemia, and hyperglycemia. An affiliation was found between the initiation of myocardial injury ailment and long term treatment with dopamine D2 agonist drugs identified with the partial activation of 5-hydroxytryptamine receptor 2 A (5-HT2A). The investigation aimed to examine the activity of sarpogrelate (a 5-HT2A receptor blocker) in reducing myocardial injury prompted by extended haul utilisation of D2 receptor agonists in rats with alloxan-induced diabetes. Methods Both bromocriptine and cabergoline were managed independently and combined with sarpogrelate for about a month in diabetic nephropathy rats. Both tail-cuff blood pressure and the BGL were recorded weekly. For all animals, the kidney hypertrophy index, serum creatinine, blood urea nitrogen, alanine transaminase, and aspartate transaminase levels were measured after one month of treatment. The severity of the cardiac injury was assessed by the estimation of lactate dehydrogenase-1 (LDH-1), cardiac troponin I, and tumor necrosis factor alpha 1 (TNF1). The triphenyltetrazolium chloride (TTC) staining method was used to determine the experimental myocardial infarction (MI) size. Results Bromocriptine and cabergoline created a significant reduction in BGL, BP, and kidney hypertrophy index in diabetic nephropathy rats. Administration of bromocriptine and cabergoline, alone, or in combination with sarpogrelate fundamentally diminished the blood concentrations of alkaline phosphatase (ALP), Aspartate aminotransferase (AST), urea, and creatinine. Bromocriptine and cabergoline alone showed a noteworthy increase in the LDH-1, Troponin I, and TNF1 levels in the serum (p < 0.05). Paradoxically, utilising bromocriptine or cabergoline with sarpogrelate treatment altogether decreased the levels of the myocardial biomarkers in the serum. A mix of bromocriptine or cabergoline with sarpogrelate diminished the level of the myocardial infarct size in the heart assessed through the TTC staining method. Conclusions The examination demonstrated that the combined use of sarpogrelate with bromocriptine or cabergoline decreased the potential adverse effects of these two drugs on the myocardial tissues.

Effect of nitroglycerin on size of an experimental myocardial infarct

1981 ◽  
Vol 92 (2) ◽  
pp. 1067-1069
Author(s):  
Yu. M. Ostrogorskii ◽  
N. I. Afonskaya ◽  
N. M. Cherpachenko ◽  
Yu. B. Rozonov ◽  
N. V. Kaverina ◽  
...  
Keyword(s):  
Myocardial Infarct ◽  
Experimental Myocardial Infarct

Determination of Experimental myocardial infarct size

1981 ◽  
Vol 6 (3) ◽  
pp. 199-210 ◽  
Author(s):  
David C. Warltier ◽  
Mark G. Zyvoloski ◽  
Garrett J. Gross ◽  
Harold F. Hardman ◽  
Harold L. Brooks
Keyword(s):  
Infarct Size ◽  
Myocardial Infarct ◽  
Myocardial Infarct Size ◽  
Experimental Myocardial Infarct

Effect of Composite Nanoparticle CeO2 on Myocardial Ischemic Re-Infusion of Cardio Myocyte Apoptosis in Mouse

2021 ◽  
Vol 21 (2) ◽  
pp. 1397-1402
Author(s):  
Chengbin Wang ◽  
Lin Ding ◽  
Jiamei Zhao ◽  
Beibei Cao ◽  
Mingwei He
Keyword(s):  
Free Radicals ◽  
Cell Membrane ◽  
Cardiac Muscle ◽  
Unsaturated Fatty Acids ◽  
Ischemia Reperfusion Injury ◽  
Cell Structure ◽  
Ischemia Reperfusion ◽  
Myocardial Tissue ◽  
R Process ◽  
Organelle Membrane

The myocardial I/R damage is very complicated. Apoptosis is considered to its a critical mechanism. During the cardiac muscle I/R process, oxygen-free radicals play a pivotal role. Arrhythmias, as well as enlargement of the area of myocardial infarction after cardiac muscle I/R process, are caused by adequate blast generated O2- ion free radicals. During the ischemia-reperfusion process, a large amount of O2- ion free radicals destroyed the cell structure, and it undergoes lipid peroxidation with unsaturated fatty acids that contain a large number of phospholipids in the cell membrane, causing membrane proteins such as ion channels and enzymes on the cell membrane. The activity of cell is reduced, which affects the function of cell membrane and organelle membrane, destroys its integrity and reduces fluidity.We observed the effects of cerium dioxide nanoparticles on glutathione peroxidase as well as superoxide dismutase, also propionate in myocardial tissue of I/R injury in the mouse. Its effects of malondialdehyde and apoptosis were explored to see its protective effect and to provide more preventive measures for ischemia-reperfusion injury.

scholarly journals Molecular Basis of Calmodulin Binding to Cardiac Muscle Ca2+Release Channel (Ryanodine Receptor)

2003 ◽  
Vol 278 (26) ◽  
pp. 23480-23486 ◽  
Author(s):  
Naohiro Yamaguchi ◽  
Le Xu ◽  
Daniel A. Pasek ◽  
Kelly E. Evans ◽  
Gerhard Meissner
Keyword(s):  
Cardiac Muscle ◽  
Ryanodine Receptor ◽  
Molecular Basis ◽  
Release Channel ◽  
Calmodulin Binding
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