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1

Khalil, Alizan A., Farah A. Aziz, and John C. Hall. "Reperfusion Injury." Plastic and Reconstructive Surgery 117, no. 3 (2006): 1024–33. http://dx.doi.org/10.1097/01.prs.0000204766.17127.54.

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2

Grinyo, J. M. "Reperfusion injury." Transplantation Proceedings 29, no. 1-2 (1997): 59–62. http://dx.doi.org/10.1016/s0041-1345(96)00715-4.

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3

Quinones-Baldrich, William J., and Deborah Caswell. "Reperfusion Injury." Critical Care Nursing Clinics of North America 3, no. 3 (1991): 525–34. http://dx.doi.org/10.1016/s0899-5885(18)30722-6.

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4

Royston, David. "Reperfusion injury." Baillière's Clinical Anaesthesiology 2, no. 3 (1988): 707–27. http://dx.doi.org/10.1016/s0950-3501(88)80014-x.

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5

Zimmerman, Barbara J., and D. Neil Granger. "Reperfusion Injury." Surgical Clinics of North America 72, no. 1 (1992): 65–83. http://dx.doi.org/10.1016/s0039-6109(16)45628-8.

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6

Reichek, Nathaniel, and Kambiz Parcham-Azad. "Reperfusion Injury." Journal of the American College of Cardiology 55, no. 12 (2010): 1206–8. http://dx.doi.org/10.1016/j.jacc.2009.10.048.

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7

Flaherty, John T., and Myron L. Weisfeldt. "Reperfusion injury." Free Radical Biology and Medicine 5, no. 5-6 (1988): 409–19. http://dx.doi.org/10.1016/0891-5849(88)90115-3.

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8

Fishbein, M. C. "Reperfusion injury." Clinical Cardiology 13, no. 3 (1990): 213–17. http://dx.doi.org/10.1002/clc.4960130312.

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9

Ma, Yulong, Yanhui Cai, Doutong Yu, et al. "Astrocytic Glycogen Mobilization in Cerebral Ischemia/Reperfusion Injury." Neuroscience and Neurological Surgery 11, no. 3 (2022): 01–05. http://dx.doi.org/10.31579/2578-8868/228.

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Glycogen is an important energy reserve in the brain and can be rapidly degraded to maintain metabolic homeostasis during cerebral blood vessel occlusion. Recent studies have pointed out the alterations in glycogen and its underlying mechanism during reperfusion after ischemic stroke. In addition, glycogen metabolism may work as a promising therapeutic target to relieve reperfusion injury. Here, we summarize the progress of glycogen metabolism during reperfusion injury and its corresponding application in patients suffering from ischemic stroke.
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10

Bodwell, Wendy. "Ischemia, reperfusion, and reperfusion injury." Journal of Cardiovascular Nursing 4, no. 1 (1989): 25–32. http://dx.doi.org/10.1097/00005082-198911000-00005.

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11

Karmazyn, Morris. "The 1990 Merck Frosst Award. Ischemic and reperfusion injury in the heart. Cellular mechanisms and pharmacological interventions." Canadian Journal of Physiology and Pharmacology 69, no. 6 (1991): 719–30. http://dx.doi.org/10.1139/y91-108.

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Reperfusion in the heart represents an important form of tissue injury, particularly in view of the emerging importance of reperfusion protocols aimed at salvaging the ischemic myocardium. Both the manifestations and the causes of reperfusion injury are multifold. With respect to the former, reperfusion injury can be characterized by various abnormalities including development of arrhythmias, contractile dysfunction, ultrastructural damage as well as various defects in intracellular biochemical homeostasis. The mechanisms underlying myocardial reperfusion injury are equally complex, but most l
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12

Songur, Çetin Murat. "Ischemia-Reperfusion Injury." Kosuyolu Heart Journal 18, no. 2 (2015): 89–93. http://dx.doi.org/10.5578/khj.5774.

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13

Yellon, Derek M., and Derek J. Hausenloy. "Myocardial Reperfusion Injury." New England Journal of Medicine 357, no. 11 (2007): 1121–35. http://dx.doi.org/10.1056/nejmra071667.

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14

Souidi, Naima, Meaghan Stolk, and Martina Seifert. "Ischemia–reperfusion injury." Current Opinion in Organ Transplantation 18, no. 1 (2013): 34–43. http://dx.doi.org/10.1097/mot.0b013e32835c2a05.

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15

Misinski, Maureen. "Myocardial Reperfusion Injury." Critical Care Nursing Clinics of North America 2, no. 4 (1990): 651–62. http://dx.doi.org/10.1016/s0899-5885(18)30785-8.

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16

AMBROSIO, G. "Myocardial reperfusion injury." European Heart Journal Supplements 4 (March 2002): B28—B30. http://dx.doi.org/10.1016/s1520-765x(02)90013-1.

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17

Ko, Wilson, Arthur S. Hawes, W. Douglas Lazenby, et al. "Myocardial reperfusion injury." Journal of Thoracic and Cardiovascular Surgery 102, no. 2 (1991): 297–308. http://dx.doi.org/10.1016/s0022-5223(19)36563-8.

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18

Huber, Thomas. "Ischaemia-reperfusion injury." Journal of Vascular Surgery 31, no. 5 (2000): 1081–82. http://dx.doi.org/10.1067/mva.2000.105513.

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19

Boyle, Edward M., Timothy H. Pohlman, Carol J. Cornejo, and Edward D. Verrier. "Ischemia-Reperfusion Injury." Annals of Thoracic Surgery 64, no. 4 (1997): S24—S30. http://dx.doi.org/10.1016/s0003-4975(97)00958-2.

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20

Olds, Robin. "Ischaemia–reperfusion injury." Pathology 31, no. 4 (1999): 444. http://dx.doi.org/10.1016/s0031-3025(16)34766-3.

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21

Tilney, N. L., D. Paz, J. Ames, M. Gasser, I. Laskowski, and W. W. Hancock. "Ischemia-reperfusion injury." Transplantation Proceedings 33, no. 1-2 (2001): 843–44. http://dx.doi.org/10.1016/s0041-1345(00)02341-1.

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22

Dorweiler, Bernhard, Diethard Pruefer, Terezia B. Andrasi, et al. "Ischemia-Reperfusion Injury." European Journal of Trauma and Emergency Surgery 33, no. 6 (2007): 600–612. http://dx.doi.org/10.1007/s00068-007-7152-z.

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23

McIntyre, Kenneth E. "ISCHAEMIA-REPERFUSION INJURY." Shock 12, no. 3 (1999): 246. http://dx.doi.org/10.1097/00024382-199909000-00019.

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24

AL-QATTAN, M. M. "Ischaemia-Reperfusion Injury." Journal of Hand Surgery 23, no. 5 (1998): 570–73. http://dx.doi.org/10.1016/s0266-7681(98)80003-x.

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Prolonged ischaemia sometimes occurs in replantation and free flap surgery. The re-establishment of circulatory flow to the ischaemic tissue leads to a cascade of events which augments tissue necrosis. This paper reviews the pathophysiology of this ischaemia-reperfusion injury and discusses different methods to modulate this injury.
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25

YAMAZAKI, NOBORU. "Myocardial reperfusion injury." Nihon Naika Gakkai Zasshi 81, no. 7 (1992): 1119–24. http://dx.doi.org/10.2169/naika.81.1119.

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26

Widgerow, Alan D. "Ischemia-Reperfusion Injury." Annals of Plastic Surgery 72, no. 2 (2014): 253–60. http://dx.doi.org/10.1097/sap.0b013e31825c089c.

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27

Grace, P. A. "Ischaemia-reperfusion injury." British Journal of Surgery 81, no. 5 (1994): 637–47. http://dx.doi.org/10.1002/bjs.1800810504.

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28

Anaya-Prado, Roberto, Luis H. Toledo-Pereyra, Alex B. Lentsch, and Peter A. Ward. "Ischemia/Reperfusion Injury." Journal of Surgical Research 105, no. 2 (2002): 248–58. http://dx.doi.org/10.1006/jsre.2002.6385.

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29

Pizarro, Gonzalo. "Ischemia Reperfusion Injury." JACC: Basic to Translational Science 8, no. 10 (2023): 1295–97. http://dx.doi.org/10.1016/j.jacbts.2023.08.009.

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30

Linas, S. L., P. F. Shanley, D. Whittenburg, E. Berger, and J. E. Repine. "Neutrophils accentuate ischemia-reperfusion injury in isolated perfused rat kidneys." American Journal of Physiology-Renal Physiology 255, no. 4 (1988): F728—F735. http://dx.doi.org/10.1152/ajprenal.1988.255.4.f728.

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The contribution of neutrophils to reperfusion injury after ischemia is not known. To determine the effect of neutrophils on the function of ischemic kidneys, we added purified human neutrophils during perfusion of isolated ischemic or nonischemic rat kidneys. Reperfusion of ischemic kidneys with neutrophils caused a distinct morphological lesion of vascular endothelial and smooth muscle cells and more functional injury than reperfusion with buffered albumin alone; with neutrophils, glomerular filtration rate (GFR) was 113 +/- 7 microliter.min-1.g-1, tubular sodium reabsorption (TNa) was 72 +/
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31

Sakuma, Tsutomu, Keiji Takahashi, Nobuo Ohya, et al. "Ischemia-reperfusion lung injury in rabbits: mechanisms of injury and protection." American Journal of Physiology-Lung Cellular and Molecular Physiology 276, no. 1 (1999): L137—L145. http://dx.doi.org/10.1152/ajplung.1999.276.1.l137.

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To study the mechanisms responsible for ischemia-reperfusion lung injury, we developed an anesthetized rabbit model in which the effects of lung deflation, lung inflation, alveolar gas composition, hypothermia, and neutrophils on reperfusion pulmonary edema could be studied. Rabbits were anesthetized and ventilated, and the left pulmonary hilum was clamped for either 2 or 4 h. Next, the left lung was reperfused and ventilated with 100% oxygen. As indexes of lung injury, we measured arterial oxygenation, extravascular lung water, and the influx of a vascular protein (131I-labeled albumin) into
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32

Rubin, B. B., S. Liauw, J. Tittley, A. D. Romaschin, and P. M. Walker. "Prolonged adenine nucleotide resynthesis and reperfusion injury in postischemic skeletal muscle." American Journal of Physiology-Heart and Circulatory Physiology 262, no. 5 (1992): H1538—H1547. http://dx.doi.org/10.1152/ajpheart.1992.262.5.h1538.

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Skeletal muscle ischemia results in energy depletion and intracellular acidosis. Reperfusion is associated with impaired adenine nucleotide resynthesis, edema formation, and myocyte necrosis. The purpose of these studies was to define the time course of cellular injury and adenine nucleotide depletion and resynthesis in postischemic skeletal muscle during prolonged reperfusion in vivo. The isolated canine gracilis muscle model was used. After 5 h of ischemia, muscles were reperfused for either 1 or 48 h. Lactate and creatine phosphokinase (CPK) release during reperfusion was calculated from ar
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33

Geng, Xiaokun, Jie Gao, Alexandra Wehbe, et al. "Reperfusion and reperfusion injury after ischemic stroke." Environmental Disease 7, no. 2 (2022): 33. http://dx.doi.org/10.4103/ed.ed_12_22.

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34

GARCIADORADO, D., and H. PIPER. "Postconditioning: Reperfusion of “reperfusion injury” after hibernation." Cardiovascular Research 69, no. 1 (2006): 1–3. http://dx.doi.org/10.1016/j.cardiores.2005.11.011.

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35

Pemberton, M., G. Anderson, V. Vĕtvicka, D. E. Justus, and G. D. Ross. "Microvascular effects of complement blockade with soluble recombinant CR1 on ischemia/reperfusion injury of skeletal muscle." Journal of Immunology 150, no. 11 (1993): 5104–13. http://dx.doi.org/10.4049/jimmunol.150.11.5104.

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Abstract Reperfusion of ischemic tissue is associated with tissue injury greater than that resulting from ischemia alone. C activation has been hypothesized to mediate the so-called ischemia/reperfusion injury through both membrane attack and C5a-dependent recruitment of neutrophils to sites of C3 fixation on the endothelium via C3 receptors. Adherence of neutrophils is preconditional to expression of their deleterious effects, which are central to the pathophysiology of ischemia/reperfusion injury. This study was designed to evaluate the effect of inhibition of C activation on ischemia/reperf
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36

Kang, K. J. "Mechanism of hepatic ischemia/reperfusion injury and protection against reperfusion injury." Transplantation Proceedings 34, no. 7 (2002): 2659–61. http://dx.doi.org/10.1016/s0041-1345(02)03465-6.

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37

Tak, Eunyoung, Gil-Chun Park, Seok-Hwan Kim, et al. "Epigallocatechin-3-gallate protects against hepatic ischaemia–reperfusion injury by reducing oxidative stress and apoptotic cell death." Journal of International Medical Research 44, no. 6 (2016): 1248–62. http://dx.doi.org/10.1177/0300060516662735.

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Objective To investigate the protective effects of epigallocatechin-3-gallate (EGCG), a major polyphenol source in green tea, against hepatic ischaemia–reperfusion injury in mice. Methods The partial hepatic ischaemia–reperfusion injury model was created by employing the hanging-weight method in C57BL/6 male mice. EGCG (50 mg/kg) was administered via an intraperitoneal injection 45 min before performing the reperfusion. A number of markers of inflammation, oxidative stress, apoptosis and liver injury were measured after the ischaemia–reperfusion injury had been induced. Results The treatment g
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38

van der Weg, Kirian, Frits W. Prinzen, and Anton PM Gorgels. "Editor’s Choice- Reperfusion cardiac arrhythmias and their relation to reperfusion-induced cell death." European Heart Journal: Acute Cardiovascular Care 8, no. 2 (2018): 142–52. http://dx.doi.org/10.1177/2048872618812148.

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Reperfusion does not only salvage ischaemic myocardium but can also cause additional cell death which is called lethal reperfusion injury. The time of reperfusion is often accompanied by ventricular arrhythmias, i.e. reperfusion arrhythmias. While both conditions are seen as separate processes, recent research has shown that reperfusion arrhythmias are related to larger infarct size. The pathophysiology of fatal reperfusion injury revolves around intracellular calcium overload and reactive oxidative species inducing apoptosis by opening of the mitochondrial protein transition pore. The pathoph
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39

Hayase, Naoki, Kent Doi, Takahiro Hiruma, et al. "Recombinant Thrombomodulin on Neutrophil Extracellular Traps in Murine Intestinal Ischemia–Reperfusion." Anesthesiology 131, no. 4 (2019): 866–82. http://dx.doi.org/10.1097/aln.0000000000002898.

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Abstract Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New Background In multiple-organ dysfunction, an injury affecting one organ remotely impacts others, and the injured organs synergistically worsen outcomes. Recently, several mediators, including extracellular histones and neutrophil extracellular traps, were identified as contributors to distant organ damage. This study aimed to elucidate whether these mediators play a crucial role in remote organ damage induced by intestinal ischemia–reperfusion. This study also aimed to evaluate the protec
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40

Wu, Meng-Yu, Giou-Teng Yiang, Wan-Ting Liao, et al. "Current Mechanistic Concepts in Ischemia and Reperfusion Injury." Cellular Physiology and Biochemistry 46, no. 4 (2018): 1650–67. http://dx.doi.org/10.1159/000489241.

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Ischemia-reperfusion injury is associated with serious clinical manifestations, including myocardial hibernation, acute heart failure, cerebral dysfunction, gastrointestinal dysfunction, systemic inflammatory response syndrome, and multiple organ dysfunction syndrome. Ischemia-reperfusion injury is a critical medical condition that poses an important therapeutic challenge for physicians. In this review article, we present recent advances focusing on the basic pathophysiology of ischemia-reperfusion injury, especially the involvement of reactive oxygen species and cell death pathways. The invol
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41

Zou, Lei, Bashir Attuwaybi та Bruce C. Kone. "Effects of NF-κB inhibition on mesenteric ischemia-reperfusion injury". American Journal of Physiology-Gastrointestinal and Liver Physiology 284, № 4 (2003): G713—G721. http://dx.doi.org/10.1152/ajpgi.00431.2002.

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Mesenteric ischemia-reperfusion injury is a serious complication of shock. Because activation of nuclear factor-κB (NF-κB) has been implicated in this process, we treated rats with vehicle or the IκB-α inhibitor BAY 11-7085 (25 mg/kg ip) 1 h before mesenteric ischemia-reperfusion (45 min of ischemia followed by reperfusion at 30 min or 6 h) and examined the ileal injury response. Vehicle-treated rats subjected to ischemia-reperfusion exhibited severe mucosal injury, increased myeloperoxidase (MPO) activity, increased expression of interleukin-6 and intercellular adhesion molecule 1 protein, an
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42

Goldfarb, R. D., and A. Singh. "GSH and reperfusion injury." Circulation 80, no. 3 (1989): 712–13. http://dx.doi.org/10.1161/circ.80.3.2766517.

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43

Mitsos, S. E., J. C. Fantone, K. P. Gallagher, et al. "Canine Myocardial Reperfusion Injury." Journal of Cardiovascular Pharmacology 8, no. 5 (1986): 978–88. http://dx.doi.org/10.1097/00005344-198609000-00015.

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44

Opie, Lionel H. "Mechanisms of reperfusion injury." Current Opinion in Cardiology 6, no. 6 (1991): 864–67. http://dx.doi.org/10.1097/00001573-199112000-00002.

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45

Ostadal, Petr. "What is ‘reperfusion injury’?" European Heart Journal 26, no. 1 (2004): 99. http://dx.doi.org/10.1093/eurheartj/ehi029.

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46

Tosaki, Arpad, Anne Hellegouarch, and Pierre Braquel. "Cicletanine and Reperfusion Injury." Journal of Cardiovascular Pharmacology 17, no. 4 (1991): 551–59. http://dx.doi.org/10.1097/00005344-199104000-00005.

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47

Weight, S. C., P. R. F. Bell, and M. L. Nicholson. "Renal ischaemia-reperfusion injury." British Journal of Surgery 83, no. 2 (1996): 162–70. http://dx.doi.org/10.1046/j.1365-2168.1996.02182.x.

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48

Rushing, G. D., and L. D. Britt. "Reperfusion Injury After Hemorrhage." Annals of Surgery 247, no. 6 (2008): 929–37. http://dx.doi.org/10.1097/sla.0b013e31816757f7.

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49

Clark, W. M. "Cytokines and reperfusion injury." Neurology 49, Issue 5, Supplement 4 (1997): S10—S14. http://dx.doi.org/10.1212/wnl.49.5_suppl_4.s10.

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50

Obermaier, Robert, Oliver Drognitz, Stefan Benz, Ulrich T. Hopt, and Przemyslaw Pisarski. "Pancreatic Ischemia/Reperfusion Injury." Pancreas 37, no. 3 (2008): 328–32. http://dx.doi.org/10.1097/mpa.0b013e31816d9283.

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