Zeitschriftenartikel: „Reperfusion injury“

1

Khalil, Alizan A., Farah A. Aziz, and John C. Hall. "Reperfusion Injury." Plastic and Reconstructive Surgery 117, no. 3 (March 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 (February 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 (September 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 (September 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 (February 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 (March 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 (January 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 (March 1990): 213–17. http://dx.doi.org/10.1002/clc.4960130312.

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9

Ma, Yulong, Yanhui Cai, Doutong Yu, Yuting Qiao, Haiyun Guo, Zejun Gao, and Li Guo. "Astrocytic Glycogen Mobilization in Cerebral Ischemia/Reperfusion Injury." Neuroscience and Neurological Surgery 11, no. 3 (February 21, 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 (November 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 (June 1, 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 likely involve numerous processes acting in concert resulting in eventual cell death. In this review, a description of various such potential mechanisms, which represent primary interests of the author, are presented. An understanding of these mechanisms has led to novel pharmacological approaches towards the protection of the reperfused myocardium. For instance, several lines of evidence implicate enhanced eicosanoid, and in particular prostaglandin, synthesis in reperfusion injury, since (1) such injury is involved with enhanced prostaglandin biosynthesis, (2) inhibition of prostaglandin synthesis with various nonsteroidal anti-inflammatory drugs attenuates injury, and (3) exogenous prostaglandins increase injury. Another intracellular process that is emerging as an important contributor to reperfusion injury in the heart is the Na+/H+ exchanger, which is most likely activated upon reperfusion. Such activation would lead to numerous intracellular disturbances including the increased synthesis of prostaglandins and elevated intracellular Ca2+ concentrations. Indeed, inhibitors of Na+/H+ exchange such as amiloride have been shown to effectively inhibit reperfusion injury. Reperfusion is also associated with depressed mitochondrial function, particularly in subsarcolemmal mitochondria which are rapidly injured as a result of both ischemic and reperfusion conditions. Preservation of mitochondrial function with dissimilar approaches such as carnitine or phosphatidylcholine administration markedly reduces reperfusion injury. A nonpharmacological novel approach towards the protection of the reperfused myocardium represents the induction of so-called stress or heart shock proteins in the heart prior to initiation of ischemia and reperfusion. The salutary effect of the heat shock response may be dependent not on the heat shock proteins themselves, but through the concomitant elevation of tissue catalase content resulting in enhanced detoxification of intracellular hydrogen peroxide. Thus reperfusion injury represents numerous complex events such that manipulations aimed at limiting such injury can be initiated to prevent specific defects with the ultimate goal of an overall reduction in cell damage.Key words: heart, ischemia, reperfusion, prostaglandins, leukotrienes, Na+/H+ exchange, subsarcolemmal mitochondria, interfibrillar mitochondria, heat shock proteins, tissue protection.

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12

Songur, Çetin Murat. "Ischemia-Reperfusion Injury." Kosuyolu Heart Journal 18, no. 2 (August 3, 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 (September 13, 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 (February 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 (December 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, Steven E. Calvano, Yong T. Shin, John A. Zelano, Anthony C. Antonacci, O. Wayne Isom, and Karl H. Krieger. "Myocardial reperfusion injury." Journal of Thoracic and Cardiovascular Surgery 102, no. 2 (August 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 (May 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 (October 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 (February 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, Sasa M. Maksan, Walther Schmiedt, Achim Neufang, and Christian F. Vahl. "Ischemia-Reperfusion Injury." European Journal of Trauma and Emergency Surgery 33, no. 6 (November 20, 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 (September 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 (October 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 (February 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 (May 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 (June 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 (October 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 (October 1, 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 +/- 2%; without neutrophils, GFR was 222 +/- 18 microliter.min-1.g-1; TNa was 90 +/- 2%; both P less than 0.01 vs. reperfusion with neutrophils. In contrast, addition of neutrophils did not injure control kidneys, unless the neutrophil activator, phorbol myristate acetate, was also added. Two experiments suggested that O2 metabolites contributed to neutrophil-mediated injury to ischemic kidneys. First, reperfusion of ischemic kidneys with O2 metabolite-deficient neutrophils from a patient with chronic granulomatous disease did not cause more injury than reperfusion with buffered albumin alone. Second, simultaneous addition of the O2 metabolite scavenger, catalase, prevented the GFR and TNa decreases caused by neutrophils but did not decrease injury in the absence of neutrophils. We conclude that neutrophils by an O2 metabolite-dependent mechanism contribute to ischemia-reperfusion injury in the isolated perfused kidney.

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31

Sakuma, Tsutomu, Keiji Takahashi, Nobuo Ohya, Osamu Kajikawa, Thomas R. Martin, Kurt H. Albertine, and Michael A. Matthay. "Ischemia-reperfusion lung injury in rabbits: mechanisms of injury and protection." American Journal of Physiology-Lung Cellular and Molecular Physiology 276, no. 1 (January 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 the extravascular space of the lungs. The principal results were that 1) all rabbits with the deflation of the lung during ischemia for 4 h died of fulminant pulmonary edema within 1 h of reperfusion; 2) inflation of the ischemic lung with either 100% oxygen, air, or 100% nitrogen prevented the reperfusion lung injury; 3) hypothermia at 6–8°C also prevented the reperfusion lung injury; 4) although circulating neutrophils declined during reperfusion lung injury, there was no increase in interleukin-8 levels in the plasma or the pulmonary edema fluid, and, furthermore, neutrophil depletion did not prevent the reperfusion injury; and 5) ultrastructural studies demonstrated injury to both the lung endothelium and the alveolar epithelium after reperfusion in deflated lungs, whereas the inflated lungs had no detectable injury. In summary, ischemia-reperfusion injury to the rabbit lung can be prevented by either hypothermia or lung inflation with either air, oxygen, or nitrogen.

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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 (May 1, 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 arteriovenous differences and blood flow. Adenine nucleotides, nucleosides, bases, and creatine phosphate were quantified by high-performance liquid chromatography, and muscle necrosis was assessed by nitroblue tetrazolium staining. Reperfusion resulted in a rapid release of lactate, which paralleled the increase in blood flow, and a delayed but prolonged release of CPK. Edema formation and muscle necrosis increased between 1 and 48 h of reperfusion (P less than 0.05). Recovery of energy stores during reperfusion was related to the extent of postischemic necrosis, which correlated with the extent of nucleotide dephosphorylation during ischemia (r = 0.88, P less than 0.001). These results suggest that both adenine nucleotide resynthesis and myocyte necrosis, which are protracted processes in reperfusing skeletal muscle, are related to the extent of nucleotide dephosphorylation during ischemia.

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Geng, Xiaokun, Jie Gao, Alexandra Wehbe, Fengwu Li, Naveed Chaudhry, Changya Peng, and Yuchuan Ding. "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 (January 2006): 1–3. http://dx.doi.org/10.1016/j.cardiores.2005.11.011.

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35

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

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36

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 (June 1, 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/reperfusion injury using a soluble and truncated recombinant human CR1 (sCR1) molecule, a "tail-less" form of the membrane C3b/C4b receptor (CD35) that functions as a regulator of C activation. Capillary perfusion and leukocyte adherence to venular endothelium were measured after reperfusion in a mouse cremaster muscle model that allowed microscopic video observation of microcirculatory changes. Infusion i.v. with sCR1 before a 4-h period of ischemia and during a 3-h subsequent period of reperfusion prevented the increase in leukocyte adherence to venular endothelium seen in controls, and enhanced the number of reperfusing capillaries by 55%. Trypan blue staining showed an increase in muscle cell viability from 11 to 50% in mice receiving sCR1 as compared to controls. Tests of blood samples from mice infused with sCR1 demonstrated nearly complete inhibition of the mouse alternative pathway of C activation, but no detectable loss of the mouse classical pathway of C activation. It was concluded that C activation in this model of skeletal muscle injury is likely to be due to the alternative pathway, and that inhibition of C activation during reperfusion inhibits leukocyte adherence to blood vessel walls and protects the capillary microcirculation.

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Tak, Eunyoung, Gil-Chun Park, Seok-Hwan Kim, Dae Young Jun, Jooyoung Lee, Shin Hwang, Gi-Won Song, and Sung-Gyu Lee. "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 (November 2, 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 groups were: sham-operated (Sham, n = 10), hepatic ischaemia–reperfusion injury (IR, n = 10), and EGCG with ischaemia–reperfusion injury (EGCG-treated IR, n = 10). Hepatic ischaemia–reperfusion injury increased the levels of biochemical and histological markers of liver injury, increased the levels of malondialdehyde, reduced the glutathione/oxidized glutathione ratio, increased the levels of oxidative stress and lipid peroxidation markers, decreased B-cell lymphoma 2 levels, and increased the levels of Bax, cytochrome c, cleaved caspase-3, and cleaved caspase-9. Pretreatment with EGCG ameliorated all of these changes. Conclusion The antioxidant and antiapoptotic effects of EGCG protected against hepatic ischaemia–reperfusion injury in mice.

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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 (November 13, 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 pathophysiological basis for reperfusion arrhythmias is the same intracellular calcium overload as that causing fatal reperfusion injury. Therefore both conditions should not be seen as separate entities but as one and the same process resulting in two different visible effects. Reperfusion arrhythmias could therefore be seen as a potential marker for fatal reperfusion injury.

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Hayase, Naoki, Kent Doi, Takahiro Hiruma, Ryo Matsuura, Yoshifumi Hamasaki, Eisei Noiri, Masaomi Nangaku, and Naoto Morimura. "Recombinant Thrombomodulin on Neutrophil Extracellular Traps in Murine Intestinal Ischemia–Reperfusion." Anesthesiology 131, no. 4 (October 1, 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 protective effects of recombinant thrombomodulin, which has been reported to neutralize extracellular histones, on multiple-organ dysfunction after intestinal ischemia–reperfusion. Methods Intestinal ischemia was induced in male C57BL/6J mice via clamping of the superior mesenteric artery. Recombinant thrombomodulin (10 mg/kg) was administered intraperitoneally with the initiation of reperfusion. The mice were subjected to a survival analysis, histologic injury scoring, quantitative polymerase chain reaction analysis of tumor necrosis factor-α and keratinocyte-derived chemokine expression, Evans blue dye vascular permeability assay, and enzyme-linked immunosorbent assay analysis of histones in the jejunum, liver, lung, and kidney after 30- or 45-min ischemia. Neutrophil extracellular trap formation was evaluated by immunofluorescence staining. Results Recombinant thrombomodulin yielded statistically significant improvements in survival after 45-min ischemia (ischemia–reperfusion without vs. with 10 mg/kg recombinant thrombomodulin: 0% vs. 33%, n = 21 per group, P = 0.001). Recombinant thrombomodulin reduced the histologic injury score, expression of tumor necrosis factor-α and keratinocyte-derived chemokine, and extravasation of Evans blue dye, which were augmented by 30-min ischemia–reperfusion, in the liver, but not in the intestine. Accumulated histones and neutrophil extracellular traps were found in the livers and intestines of 30-min ischemia–reperfusion–injured mice. Recombinant thrombomodulin reduced these accumulations only in the liver. Conclusions Recombinant thrombomodulin improved the survival of male mice with intestinal ischemia–reperfusion injury. These findings suggest that histone and neutrophil extracellular trap accumulation exacerbate remote liver injury after intestinal ischemia–reperfusion. Recombinant thrombomodulin may suppress these accumulations and attenuate liver injury.

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Wu, Meng-Yu, Giou-Teng Yiang, Wan-Ting Liao, Andy Po-Yi Tsai, Yeung-Leung Cheng, Pei-Wen Cheng, Chia-Ying Li, and Chia-Jung Li. "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 involvement of the NADPH oxidase system, nitric oxide synthase system, and xanthine oxidase system are also described. When the blood supply is re-established after prolonged ischemia, local inflammation and ROS production increase, leading to secondary injury. Cell damage induced by prolonged ischemia-reperfusion injury may lead to apoptosis, autophagy, necrosis, and necroptosis. We highlight the latest mechanistic insights into reperfusion-injury-induced cell death via these different processes. The interlinked signaling pathways of cell death could offer new targets for therapeutic approaches. Treatment approaches for ischemia-reperfusion injury are also reviewed. We believe that understanding the pathophysiology ischemia-reperfusion injury will enable the development of novel treatment interventions.

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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 (1 квітня 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, and a biphasic peak of NF-κB DNA-binding activity during the 30-min and 6-h reperfusion courses. In contrast, BAY 11-7085-pretreated rats subjected to ischemia-reperfusion exhibited less histological injury and less interleukin-6 and intercellular adhesion molecule 1 protein expression at 30 min of reperfusion but more histological injury at 6 h of reperfusion than vehicle-treated rats subjected to ischemia-reperfusion. Studies with phosphorylation site-specific antibodies demonstrated that IκB-α phosphorylation at Ser32,Ser36 was induced at 30 min of reperfusion, whereas tyrosine phosphorylation of IκB-α was induced at 6 h of reperfusion. BAY 11-7085 inhibited the former, but not the latter, phosphorylation pathway, whereas α-melanocyte-stimulating hormone, which is effective in limiting late ischemia-reperfusion injury to the intestine, inhibited tyrosine phosphorylation of IκB-α. Thus NF-κB appears to play an important role in the generation and resolution of intestinal ischemia-reperfusion injury through different activation pathways.

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

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Mitsos, S. E., J. C. Fantone, K. P. Gallagher, K. M. Walden, P. J. Simpson, G. D. Abrams, M. A. Schork, and B. R. Lucchesi. "Canine Myocardial Reperfusion Injury." Journal of Cardiovascular Pharmacology 8, no. 5 (September 1986): 978–88. http://dx.doi.org/10.1097/00005344-198609000-00015.

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

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Ostadal, Petr. "What is ‘reperfusion injury’?" European Heart Journal 26, no. 1 (November 30, 2004): 99. http://dx.doi.org/10.1093/eurheartj/ehi029.

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

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

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

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Clark, W. M. "Cytokines and reperfusion injury." Neurology 49, Issue 5, Supplement 4 (November 1, 1997): S10—S14. http://dx.doi.org/10.1212/wnl.49.5_suppl_4.s10.

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

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