VEGF 165 transfection decreases postischemic NF‐κB‐dependent myocardial reperfusion injury in vivo: role of eNOS phosphorylation

2003 ◽  
Vol 17 (6) ◽  
pp. 705-707 ◽  
Author(s):  
Christian Kupatt ◽  
Rabea Hinkel ◽  
Robert Vachenauer ◽  
Jan Horstkotte ◽  
Philip Raake ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Myocardial Reperfusion ◽  
Myocardial Reperfusion Injury ◽  
Enos Phosphorylation

The Role of Non-coding RNAs in Ischemic Myocardial Reperfusion Injury

2019 ◽  
Vol 33 (4) ◽  
pp. 489-498 ◽  
Author(s):  
Vince Siebert ◽  
Joseph Allencherril ◽  
Yumei Ye ◽  
Xander H. T. Wehrens ◽  
Yochai Birnbaum
Keyword(s):  
Reperfusion Injury ◽  
Myocardial Reperfusion ◽  
Myocardial Reperfusion Injury ◽  
Non Coding Rnas

Myocardial reperfusion injury management: erythropoietin compared with postconditioning

2009 ◽  
Vol 297 (6) ◽  
pp. H2035-H2043 ◽  
Author(s):  
Sophie Tamareille ◽  
Nehmat Ghaboura ◽  
Frederic Treguer ◽  
Dalia Khachman ◽  
Anne Croué ◽  
...  
Keyword(s):  
Infarct Size ◽  
Reperfusion Injury ◽  
Isolated Heart ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Myocardial Reperfusion ◽  
Myocardial Reperfusion Injury ◽  
Gsk 3Β ◽  
Developed Pressure

Ischemic postconditioning (IPost) and erythropoietin (EPO) have been shown to attenuate myocardial reperfusion injury using similar signaling pathways. The aim of this study was to examine whether EPO is as effective as IPost in decreasing postischemic myocardial injury in both Langendorff-isolated-heart and in vivo ischemia-reperfusion rat models. Rat hearts were subjected to 25 min ischemia, followed by 30 min or 2 h of reperfusion in the isolated-heart study. Rats underwent 45 min ischemia, followed by 24 h of reperfusion in the in vivo study. In both studies, the control group ( n = 12; ischemia-reperfusion only) was compared with IPost ( n = 16; 3 cycles of 10 s reperfusion/10 s ischemia) and EPO ( n = 12; 1,000 IU/kg) at the onset of reperfusion. The following resulted. First, in the isolated hearts, IPost or EPO significantly improved postischemic recovery of left ventricular developed pressure. EPO induced better left ventricular developed pressure than IPost at 30 min of reperfusion (73.18 ± 10.23 vs. 48.11 ± 7.92 mmHg, P < 0.05). After 2 h of reperfusion, the infarct size was significantly lower in EPO-treated hearts compared with IPost and control hearts (14.36 ± 0.60%, 19.11 ± 0.84%, and 36.21 ± 4.20% of the left ventricle, respectively; P < 0.05). GSK-3β phosphorylation, at 30 min of reperfusion, was significantly higher with EPO compared with IPost hearts. Phosphatidylinositol 3-kinase and ERK1/2 inhibitors abolished both EPO- and IPost-mediated cardioprotection. Second, in vivo, IPost and EPO induced an infarct size reduction compared with control (40.5 ± 3.6% and 28.9 ± 3.1%, respectively, vs. 53.7 ± 4.3% of the area at risk; P < 0.05). Again, EPO decreased significantly more infarct size and transmurality than IPost ( P < 0.05). In conclusion, with the use of our protocols, EPO showed better protective effects than IPost against reperfusion injury through higher phosphorylation of GSK-3β.

Factors modifying protective effect of anti-CD18 antibodies on myocardial reperfusion injury in dogs

1996 ◽  
Vol 270 (1) ◽  
pp. H53-H64 ◽  
Author(s):  
R. G. Perez ◽  
M. Arai ◽  
C. Richardson ◽  
A. DiPaula ◽  
C. Siu ◽  
...  
Keyword(s):  
Infarct Size ◽  
Reperfusion Injury ◽  
Myocardial Reperfusion ◽  
Myocardial Reperfusion Injury ◽  
H2o2 Production ◽  
Myeloperoxidase Activity ◽  
Collateral Flow ◽  
Severe Ischemia

Anti-CD18 monoclonal antibodies (MAb) have demonstrated variable protection against neutrophil (PMN)-mediated myocardial reperfusion injury. To identify factors contributing to this variability, open-chest dogs underwent coronary artery occlusion for 90 min followed by reperfusion for 3.5 h. Ten minutes before reperfusion the dogs received saline (n = 18) or one of three anti-CD18 MAb: MHM.23, R15.7, or PLM-2 (2, 1, and 1 mg/kg and n = 19, 8, and 4, respectively). Collateral flow was measured with radioactive microspheres, area at risk was assessed with monastral blue dye, and infarct size was measured postmortem by triphenyltetrazolium chloride. In vitro, all three MAb bound to canine PMNs, but only MHM.23 and R15.7 inhibited their adherence to keyhole limpet hemocyanin-coated plastic. In vivo, only MHM.23 and R15.7 significantly reduced infarct size after adjusting for the effect of collateral flow. MHM.23 afforded protection in dogs with moderate ischemia (epicardial collateral flow > 0.1 ml.min-1.g-1, infarct size reduced 46%) but not in dogs with more severe ischemia. Only R15.7 was effective in dogs with severe ischemia. Although MHM.23 and R15.7 produced similar inhibition of tissue PMN accumulation, as reflected by myeloperoxidase activity. R15.7 markedly inhibited H2O2 production by PMNs after exposure to platelet-activating factor, whereas MHM.23 had only a minimal effect. The effectiveness of different anti-CD18 MAb in preventing reperfusion injury appears to be 1) highly dependent on the specific anti-CD18 MAb employed, 2) predicted only partially by in vitro binding to PMNs, static in vitro tests of PMN adherence, or the extent of inhibition of PMN accumulation in vivo, 3) related more to their ability to inhibit oxidant release from activated PMNs, and 4) strongly influenced by the severity of myocardial ischemia before reperfusion.

scholarly journals Role of Oxygen Free Radicals and Arachldonate Lipoxygenase Metabolism in Myocardial Reperfusion Injury.

1991 ◽  
Vol 55 ◽  
pp. 39
Author(s):  
Tsunehiko Kuzuya ◽  
Shiro Hoshida ◽  
Youngjoon Kim ◽  
Hisakazu Fuji ◽  
Hiroshi Ohe ◽  
...  
Keyword(s):  
Free Radicals ◽  
Reperfusion Injury ◽  
Oxygen Free Radicals ◽  
Myocardial Reperfusion ◽  
Myocardial Reperfusion Injury
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