Myocardial reperfusion injury. N Engl J Med

Hatter Cardiovascular Institute, University College London Hospital and Medical School, London, United Kingdom.
New England Journal of Medicine (Impact Factor: 55.87). 10/2007; 357(11):1121-35. DOI: 10.1056/NEJMra071667
Source: PubMed


Lethal reperfusion injury is a paradoxical type of myocardial injury caused by the restoration of coronary blood flow after an ischemic episode. This review focuses on the mechanisms of the injury, on attempts to protect the heart against it, and on promising new approaches to cardioprotection during percutaneous coronary intervention.

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    • "Myocardial infarction is a leading cause of morbidity and mortality worldwide [1] [2]. Myocardial infarction triggers a sequence of inflammatory reactions involving the infiltration, activation, apoptosis, and clearance of neutrophils [3]. "

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    • "Myocardial infarction is a leading cause of morbidity and mortality worldwide [1] [2]. Myocardial infarction triggers a sequence of inflammatory reactions involving the infiltration, activation, apoptosis, and clearance of neutrophils [3]. "
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    ABSTRACT: Leukotriene B4 12-hydroxydehydrogenase (LTB4DH) catalyzes the oxidation of proinflammatory LTB4 into less bioactive 12-oxo-LTB4. We recently discovered that LTB4DH was induced by two different natural products in combination. We previously isolated gallic acid from Radix Paeoniae through a bioactivity-guided fractionation procedure. The purpose of this study is to test the hypothesis that LTB4DH inducers may suppress neutrophil-mediated inflammation in myocardial infarction. We first isolated the active compound(s) from another plant, Radix Astragali , by the similar strategy. By evaluating LTB4DH induction, we identified calycosin and formononetin from Radix Astragali by HPLC-ESI-MS technique. We confirmed that gallic acid and commercial calycosin or formononetin could synergistically induce LTB4DH expression in HepG2 cells and human neutrophils. Moreover, calycosin and gallic acid attenuated the effects of LTB4 on the survival and chemotaxis of neutrophil cell culture. We further demonstrated that calycosin and gallic acid synergistically suppressed neutrophil infiltration and protected cardiac integrity in the isoproterenol-induced mice model of myocardial infarction. Calycosin and gallic acid dramatically suppressed isoproterenol-induced increase in myeloperoxidase (MPO) activity and malondialdehyde (MDA) level. Collectively, our results suggest that LTB4DH inducers (i.e., calycosin and gallic acid) may be a novel combined therapy for the treatment of neutrophil-mediated myocardial injury.
    Oxidative Medicine and Cellular Longevity 08/2015; 2015(24):434052. DOI:10.1155/2015/434052 · 3.36 Impact Factor
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    • "Mechanisms for induced tissue injury mainly occur because of reactive oxygen species (ROS) formation when tissue perfusion is restored, which can lead to lethal cell injury. Currently, there is not a drug regimen that can satisfactorily avoid the deleterious consequences of IR [1] [2]. "
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    ABSTRACT: Remote ischemic conditioning (RIC) is the most promising surgical approach to mitigate ischemia and reperfusion (IR) injury. It consists in performing brief cycles of IR in tissues other than those exposed to ischemia. The underlying mechanisms of the induced protection are barely understood, so we evaluated if RIC works enhancing the antioxidant defense of the liver and kidney before IR injury. Twenty-one Wistar rats were assigned into three groups as follows: sham, same surgical procedure as in the remaining groups was performed, but no RIC was carried out. RIC 10, RIC was performed, and no abdominal organ ischemia was induced. After 10 min of the end of the RIC protocol, the liver and kidney were harvested. RIC 60, similar procedure as performed in RIC 10, but the liver and the kidney were harvested 60 min. RIC consisted of three cycles of 5-min left hind limb ischemia followed by 5-min left hind limb perfusion, lasting 30 min in total. Samples were used to measure tissue total antioxidant capacity. RIC protocol increased both liver (1.064 ± 0.26 mM/L) and kidney (1.310 ± 0.17 mM/L) antioxidant capacity after 10 min when compared with sham (liver, 0.759 ± 0.10 mM/L and kidney, 1.08 ± 0.15 mM/L). Sixty minutes after the RIC protocol, no enhancement on liver (0.687 ± 0.13 mM/L) or kidney (1.09 ± 0.15 mM/L) antioxidant capacity was detected. RIC works through temporary and short-term enhancement of liver and kidney cells antioxidant defenses to avoid the deleterious consequences of a future IR injury. Copyright © 2015 Elsevier Inc. All rights reserved.
    Journal of Surgical Research 07/2015; DOI:10.1016/j.jss.2015.07.031 · 1.94 Impact Factor
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