scholarly journals Effects of mycophenolate mofetil on acute ischaemia-reperfusion injury in rats and its consequences in the long term

2009 ◽  
Vol 25 (5) ◽  
pp. 1443-1450 ◽  
Author(s):  
M. Sabbatini ◽  
F. Uccello ◽  
V. Serio ◽  
G. Troncone ◽  
V. Varone ◽  
...  
Keyword(s):  
Mycophenolate Mofetil ◽  
Reperfusion Injury ◽  
Ischaemia Reperfusion Injury ◽  
Acute Ischaemia ◽  
Ischaemia Reperfusion

An Introduction to Cardioprotection

2011 ◽  
Keyword(s):  
Reperfusion Injury ◽  
Myocardial Injury ◽  
Artery Bypass ◽  
Bypass Graft ◽  
Myocardial Damage ◽  
Myocardial Salvage ◽  
Ischaemia Reperfusion Injury ◽  
Acute Ischaemia ◽  
Ischaemia Reperfusion ◽  
Considerable Morbidity

• In its broadest sense, the term ‘cardioprotection’ encompasses ‘all mechanisms and means that contribute to the preservation of the heart by reducing or even preventing myocardial damage’• However, for the purposes of this book, the term ‘cardioprotection’ will refer to the endogenous mechanisms and therapeutic strategies that reduce or prevent myocardial damage induced by acute ischaemia-reperfusion injury• In this context, cardioprotection begins with the primary prevention of coronary heart disease and includes the reduction of myocardial injury sustained during coronary artery bypass graft surgery, and an acute myocardial infarction, conditions with considerable morbidity and mortality• An understanding of the pathophysiology of acute myocardial ischaemia-reperfusion injury is essential when designing new cardioprotective strategies• Several methods exist for both quantifying myocardial damage induced by acute ischaemia-reperfusion injury and for assessing myocardial salvage following the application of cardioprotective strategies• Importantly, novel cardioprotective strategies must be capable of preventing and reducing myocardial damage over and above that provided by current optimal therapy.

scholarly journals Mycophenolate mofetil attenuates uterine ischaemia/reperfusion injury in a rat model

2017 ◽  
Vol 34 (2) ◽  
pp. 115-123 ◽  
Author(s):  
Gulcin Sahin Ersoy ◽  
Meryem Kurek Eken ◽  
Ozge Cevik ◽  
Ozlem T. Cilingir ◽  
Reshef Tal
Keyword(s):  
Mycophenolate Mofetil ◽  
Reperfusion Injury ◽  
Rat Model ◽  
Ischaemia Reperfusion Injury ◽  
Ischaemia Reperfusion

scholarly journals e0141 The effects and mechanisms between DIDS and EDRV on acute ischaemia-reperfusion injury myocardium

Heart ◽  
2010 ◽  
Vol 96 (Suppl 3) ◽  
pp. A45-A45
Author(s):  
L. Yan-xia ◽  
L. Jia-ni ◽  
S. Ming-zhi ◽  
Z. Meng ◽  
Z. Ya-li ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischaemia Reperfusion Injury ◽  
Acute Ischaemia ◽  
Ischaemia Reperfusion

Akt protects the heart against ischaemia-reperfusion injury by modulating mitochondrial morphology

2015 ◽  
Vol 113 (03) ◽  
pp. 513-521 ◽  
Author(s):  
Sang-Bing Ong ◽  
Andrew Hall ◽  
Rachel Dongworth ◽  
Siavash Kalkhoran ◽  
Aswin Pyakurel ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Mitochondrial Permeability Transition ◽  
Cardiac Cells ◽  
Mitochondrial Morphology ◽  
Myocardial Infarct Size ◽  
Ischaemia Reperfusion Injury ◽  
Acute Ischaemia ◽  
Mptp Opening ◽  
Ischaemia Reperfusion ◽  
Mitochondrial Elongation

SummaryThe mechanism through which the protein kinase Akt (also called PKB), protects the heart against acute ischaemia-reperfusion injury (IRI) is not clear. Here, we investigate whether Akt mediates its cardioprotective effect by modulating mitochondrial morphology. Transfection of HL-1 cardiac cells with constitutively active Akt (caAkt) changed mitochondrial morphology as evidenced by an increase in the proportion of cells displaying predominantly elongated mitochondria (73 ± 5.0 % caAkt vs 49 ± 5.8 % control: N=80 cells/group; p< 0.05). This effect was associated with delayed time taken to induce mitochondrial permeability transition pore (MPTP) opening (by 2.4 ± 0.5 fold; N=80 cells/group: p< 0.05); and reduced cell death following simulated IRI (32.8 ± 1.2 % caAkt vs 63.8 ± 5.6 % control: N=320 cells/group: p< 0.05). Similar effects on mitochondrial morphology, MPTP opening, and cell survival post-IRI, were demonstrated with pharmacological activation of Akt using the known cardioprotective cytokine, erythropoietin (EPO). The effect of Akt on inducing mitochondrial elongation was found to be dependent on the mitochondrial fusion protein, Mitofusin-1 (Mfn1), as ablation of Mfn1 in mouse embryonic fibroblasts (MEFs) abrogated Akt-mediated mitochondrial elongation. Finally, in vivo pre-treatment with EPO reduced myocardial infarct size (as a % of the area at risk) in adult mice subjected to IRI (26.2 ± 2.6 % with EPO vs 46.1 ± 6.5 % in control; N=7/group: p< 0.05), and reduced the proportion of cells displaying myofibrillar disarray and mitochondrial fragmentation observed by electron microscopy in adult murine hearts subjected to ischaemia from 5.8 ± 1.0 % to 2.2 ± 1.0 % (N=5 hearts/group; p< 0.05). In conclusion, we found that either genetic or pharmacological activation of Akt protected the heart against acute ischaemia-reperfusion injury by modulating mitochondrial morphology.

scholarly journals Sustained Isoprostane E2 Elevation, Inflammation and Fibrosis after Acute Ischaemia-Reperfusion Injury Are Reduced by Pregnane X Receptor Activation

PLoS ONE ◽  
2015 ◽  
Vol 10 (8) ◽  
pp. e0136173 ◽  
Author(s):  
Aimen O. Amer ◽  
Philip M. Probert ◽  
Michael Dunn ◽  
Margaret Knight ◽  
Abigail E. Vallance ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Pregnane X Receptor ◽  
Receptor Activation ◽  
Ischaemia Reperfusion Injury ◽  
Acute Ischaemia ◽  
Ischaemia Reperfusion
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