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Journal articles on the topic 'Reperfusion injury Pathophysiology'

Author: Grafiati

Published: 4 June 2021

Last updated: 29 January 2023

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1

Kaszaki, J., A. Wolfárd, L. Szalay, and M. Boros. "Pathophysiology of Ischemia-Reperfusion Injury." Transplantation Proceedings 38, no. 3 (April 2006): 826–28. http://dx.doi.org/10.1016/j.transproceed.2006.02.152.

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2

Carden, Donna L., and D. Neil Granger. "Pathophysiology of ischaemia-reperfusion injury." Journal of Pathology 190, no. 3 (February 2000): 255–66. http://dx.doi.org/10.1002/(sici)1096-9896(200002)190:3<255::aid-path526>3.0.co;2-6.

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3

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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4

Ildefonso, José Ángel, and Javier Arias-Díaz. "Pathophysiology of liver ischemia—Reperfusion injury." Cirugía Española (English Edition) 87, no. 4 (January 2010): 202–9. http://dx.doi.org/10.1016/s2173-5077(10)70049-1.

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5

McMichael, Maureen, and Rustin M. Moore. "Ischemia-reperfusion injury pathophysiology, part I." Journal of Veterinary Emergency and Critical Care 14, no. 4 (December 2004): 231–41. http://dx.doi.org/10.1111/j.1476-4431.2004.04004.x.

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6

PIPER, H. M. "Myocardial Protection. The Pathophysiology of Reperfusion and Reperfusion Injury." Cardiovascular Research 27, no. 1 (January 1, 1993): 142–43. http://dx.doi.org/10.1093/cvr/27.1.142a.

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7

Walker, Paul M. "Myocardial protection: The pathophysiology of reperfusion and reperfusion injury." Journal of Vascular Surgery 17, no. 4 (April 1993): 811. http://dx.doi.org/10.1016/0741-5214(93)90136-a.

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8

Rice, William G. "Myocardial protection: The pathophysiology of reperfusion and reperfusion injury." Free Radical Biology and Medicine 13, no. 4 (October 1992): 463–64. http://dx.doi.org/10.1016/0891-5849(92)90190-r.

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9

McCloskey, Gerard. "Myocardial protection: The pathophysiology of reperfusion and reperfusion injury." Journal of Cardiothoracic and Vascular Anesthesia 7, no. 4 (August 1993): 499. http://dx.doi.org/10.1016/1053-0770(93)90194-p.

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10

de Bono, David. "Myocardial protection: the pathophysiology of reperfusion and reperfusion injury." International Journal of Cardiology 35, no. 3 (June 1992): 429. http://dx.doi.org/10.1016/0167-5273(92)90250-7.

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11

Osarogiagbon, U. Raymond, Stephana Choong, John D. Belcher, Gregory M. Vercellotti, Mark S. Paller, and Robert P. Hebbel. "Reperfusion injury pathophysiology in sickle transgenic mice." Blood 96, no. 1 (July 1, 2000): 314–20. http://dx.doi.org/10.1182/blood.v96.1.314.

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Abstract Reperfusion of tissues after interruption of their vascular supply causes free-radical generation that leads to tissue damage, a scenario referred to as “reperfusion injury.” Because sickle disease involves repeated transient ischemic episodes, we sought evidence for excessive free-radical generation in sickle transgenic mice. Compared with normal mice, sickle mice at ambient air had a higher ethane excretion (marker of lipid peroxidation) and greater conversion of salicylic acid to 2,3-dihydroxybenzoic acid (marker of hydroxyl radical generation). During hypoxia (11% O2), only sickle mice converted tissue xanthine dehydrogenase to oxidase. Only the sickle mice exhibited a further increase in ethane excretion during restitution of normal oxygen tension after 2 hours of hypoxia. Only the sickle mice showed abnormal activation of nuclear factor–κB after exposure to hypoxia-reoxygenation. Allopurinol, a potential therapeutic agent, decreased ethane excretion in the sickle mice. Thus, sickle transgenic mice exhibit biochemical footprints consistent with excessive free-radical generation even at ambient air and following a transient induction of enhanced sickling. We suggest that reperfusion injury physiology may contribute to the evolution of the chronic organ damage characteristic of sickle cell disease. If so, novel therapeutic approaches might be of value.

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12

Osarogiagbon, U. Raymond, Stephana Choong, John D. Belcher, Gregory M. Vercellotti, Mark S. Paller, and Robert P. Hebbel. "Reperfusion injury pathophysiology in sickle transgenic mice." Blood 96, no. 1 (July 1, 2000): 314–20. http://dx.doi.org/10.1182/blood.v96.1.314.013k39_314_320.

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Reperfusion of tissues after interruption of their vascular supply causes free-radical generation that leads to tissue damage, a scenario referred to as “reperfusion injury.” Because sickle disease involves repeated transient ischemic episodes, we sought evidence for excessive free-radical generation in sickle transgenic mice. Compared with normal mice, sickle mice at ambient air had a higher ethane excretion (marker of lipid peroxidation) and greater conversion of salicylic acid to 2,3-dihydroxybenzoic acid (marker of hydroxyl radical generation). During hypoxia (11% O2), only sickle mice converted tissue xanthine dehydrogenase to oxidase. Only the sickle mice exhibited a further increase in ethane excretion during restitution of normal oxygen tension after 2 hours of hypoxia. Only the sickle mice showed abnormal activation of nuclear factor–κB after exposure to hypoxia-reoxygenation. Allopurinol, a potential therapeutic agent, decreased ethane excretion in the sickle mice. Thus, sickle transgenic mice exhibit biochemical footprints consistent with excessive free-radical generation even at ambient air and following a transient induction of enhanced sickling. We suggest that reperfusion injury physiology may contribute to the evolution of the chronic organ damage characteristic of sickle cell disease. If so, novel therapeutic approaches might be of value.

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13

Bulkley, Gregory B. "Pathophysiology of free radical—mediated reperfusion injury." Journal of Vascular Surgery 5, no. 3 (March 1987): 512–17. http://dx.doi.org/10.1016/0741-5214(87)90085-1.

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14

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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15

Panisello-Roselló, Arnau, and Joan Roselló-Catafau. "Molecular Mechanisms and Pathophysiology of Ischemia-Reperfusion Injury." International Journal of Molecular Sciences 19, no. 12 (December 18, 2018): 4093. http://dx.doi.org/10.3390/ijms19124093.

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16

Crinnion, J. N., S. Homer-Vanniasinkam, and M. J. Gough. "Skeletal Muscle Reperfusion Injury: Pathophysiology and Clinical Considerations." Cardiovascular Surgery 1, no. 4 (August 1993): 317–24. http://dx.doi.org/10.1177/096721099300100402.

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Skeletal muscle reperfusion injury following revascularization of an acutely ischaemic limb undoubtedly contributes to the morbidity and mortality of this surgical emergency. This article reviews the experimental evidence which has defined the biochemical events responsible for the pathogenesis of this injury, with particular emphasis on the roles played by free radicals, neutrophils and products of lipid peroxidation. Finally, the clinical relevance of both the local and systemic effects of the injury is considered, together with suggestions for potential therapeutic strategies based on the results of laboratory work.

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17

Parlakpinar, Hakan, MH Orum, and M. Sagir. "Pathophysiology of Myocardial Ischemia Reperfusion Injury: A Review." Medicine Science | International Medical Journal 2, no. 4 (2013): 935. http://dx.doi.org/10.5455/medscience.2013.02.8082.

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18

Bulkley, Gregory B. "Pathophysiology of free radical[mdash ]mediated reperfusion injury." Journal of Vascular Surgery 5, no. 3 (March 1987): 512–17. http://dx.doi.org/10.1067/mva.1987.avs0050512b.

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19

Papageorgiou, Nikolaos, Alexandros Briasoulis, and Dimitris Tousoulis. "Ischemia-reperfusion injury: Complex pathophysiology with elusive treatment." Hellenic Journal of Cardiology 59, no. 6 (November 2018): 329–30. http://dx.doi.org/10.1016/j.hjc.2018.11.002.

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20

Weigand, Kilian, Sylvia Brost, Niels Steinebrunner, Markus Büchler, Peter Schemmer, and Martina Müller. "Ischemia/Reperfusion Injury in Liver Surgery and Transplantation: Pathophysiology." HPB Surgery 2012 (May 30, 2012): 1–8. http://dx.doi.org/10.1155/2012/176723.

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Liver ischemia/reperfusion (IR) injury is caused by a heavily toothed network of interactions of cells of the immune system, cytokine production, and reduced microcirculatory blood flow in the liver. These complex networks are further elaborated by multiple intracellular pathways activated by cytokines, chemokines, and danger-associated molecular patterns. Furthermore, intracellular ionic disturbances and especially mitochondrial disorders play an important role leading to apoptosis and necrosis of hepatocytes in IR injury. Overall, enhanced production of reactive oxygen species, found very early in IR injury, plays an important role in liver tissue damage at several points within these complex networks. Many contributors to IR injury are only incompletely understood so far. This paper tempts to give an overview of the different mechanisms involved in the formation of IR injury. Only by further elucidation of these complex mechanisms IR injury can be understood and possible therapeutic strategies can be improved or be developed.

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21

Sanada, Shoji, Issei Komuro, and Masafumi Kitakaze. "Pathophysiology of myocardial reperfusion injury: preconditioning, postconditioning, and translational aspects of protective measures." American Journal of Physiology-Heart and Circulatory Physiology 301, no. 5 (November 2011): H1723—H1741. http://dx.doi.org/10.1152/ajpheart.00553.2011.

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Heart diseases due to myocardial ischemia, such as myocardial infarction or ischemic heart failure, are major causes of death in developed countries, and their number is unfortunately still growing. Preliminary exploration into the pathophysiology of ischemia-reperfusion injury, together with the accumulation of clinical evidence, led to the discovery of ischemic preconditioning, which has been the main hypothesis for over three decades for how ischemia-reperfusion injury can be attenuated. The subcellular pathophysiological mechanism of ischemia-reperfusion injury and preconditioning-induced cardioprotection is not well understood, but extensive research into components, including autacoids, ion channels, receptors, subcellular signaling cascades, and mitochondrial modulators, as well as strategies for modulating these components, has made evolutional progress. Owing to the accumulation of both basic and clinical evidence, the idea of ischemic postconditioning with a cardioprotective potential has been discovered and established, making it possible to apply this knowledge in the clinical setting after ischemia-reperfusion insult. Another a great outcome has been the launch of translational studies that apply basic findings for manipulating ischemia-reperfusion injury into practical clinical treatments against ischemic heart diseases. In this review, we discuss the current findings regarding the fundamental pathophysiological mechanisms of ischemia-reperfusion injury, the associated protective mechanisms of ischemic pre- and postconditioning, and the potential seeds for molecular, pharmacological, or mechanical treatments against ischemia-reperfusion injury, as well as subsequent adverse outcomes by modulation of subcellular signaling mechanisms (especially mitochondrial function). We also review emerging translational clinical trials and the subsistent clinical comorbidities that need to be overcome to make these trials applicable in clinical medicine.

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22

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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23

Collard, Charles D., and Simon Gelman. "Pathophysiology, Clinical Manifestations, and Prevention of Ischemia-Reperfusion Injury." Anesthesiology 94, no. 6 (June 1, 2001): 1133–38. http://dx.doi.org/10.1097/00000542-200106000-00030.

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24

Liu, Jiaqi, Haijuan Wang, and Jun Li. "Inflammation and Inflammatory Cells in Myocardial Infarction and Reperfusion Injury: A Double-Edged Sword." Clinical Medicine Insights: Cardiology 10 (January 2016): CMC.S33164. http://dx.doi.org/10.4137/cmc.s33164.

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Myocardial infarction (MI) is the most common cause of cardiac injury, and subsequent reperfusion further enhances the activation of innate and adaptive immune responses and cell death programs. Therefore, inflammation and inflammatory cell infiltration are the hallmarks of MI and reperfusion injury. Ischemic cardiac injury activates the innate immune response via toll-like receptors and upregulates chemokine and cytokine expressions in the infarcted heart. The recruitment of inflammatory cells is a dynamic and superbly orchestrated process. Sequential infiltration of the injured myocardium with neutrophils, monocytes and their descendant macrophages, dendritic cells, and lymphocytes contributes to the initiation and resolution of inflammation, infarct healing, angiogenesis, and ventricular remodeling. Both detrimental effects and a beneficial role in the pathophysiology of MI and reperfusion injury may be attributed to the subset heterogeneity and functional diversity of these inflammatory cells.

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25

Cerqueira, Nereide Freire, Carlos Alberto Hussni, and Winston Bonetti Yoshida. "Pathophysiology of mesenteric ischemia/reperfusion: a review." Acta Cirurgica Brasileira 20, no. 4 (August 2005): 336–43. http://dx.doi.org/10.1590/s0102-86502005000400013.

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During ischemia, the cell structures are progressively damaged, but restoration of the blood flow, paradoxically, intensifies the lesions caused by the ischemia. The mechanisms of ischemia injury and reperfusion (I/R) have not been completely defined and many studies have been realized in an attempt to find an ideal therapy for mesenteric I/R. The occlusion and reperfusion of the splanchnic arteries provokes local and systemic alterations principally derived from the release of cytotoxic substances and the interaction between neutrophils and endothelial cells. Substances involved in the process are discussed in the present review, like oxygen-derived free radicals, nitric oxide, transcription factors, complement system, serotonin and pancreatic proteases. The mechanisms of apoptosis, alterations in other organs, therapeutic and evaluation methods are also discussed.

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26

Nastos, Constantinos, Konstantinos Kalimeris, Nikolaos Papoutsidakis, Marios-Konstantinos Tasoulis, Panagis M. Lykoudis, Kassiani Theodoraki, Despoina Nastou, Vassilios Smyrniotis, and Nikolaos Arkadopoulos. "Global Consequences of Liver Ischemia/Reperfusion Injury." Oxidative Medicine and Cellular Longevity 2014 (2014): 1–13. http://dx.doi.org/10.1155/2014/906965.

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Liver ischemia/reperfusion injury has been extensively studied during the last decades and has been implicated in the pathophysiology of many clinical entities following hepatic surgery and transplantation. Apart from its pivotal role in the pathogenesis of the organ’s post reperfusion injury, it has also been proposed as an underlying mechanism responsible for the dysfunction and injury of other organs as well. It seems that liver ischemia and reperfusion represent an event with “global” consequences that influence the function of many remote organs including the lung, kidney, intestine, pancreas, adrenals, and myocardium among others. The molecular and clinical manifestation of these remote organs injury may lead to the multiple organ dysfunction syndrome, frequently encountered in these patients. Remote organ injury seems to be in part the result of the oxidative burst and the inflammatory response following reperfusion. The present paper aims to review the existing literature regarding the proposed mechanisms of remote organ injury after liver ischemia and reperfusion.

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27

Horwitz, Lawrence D., and Eli A. Rosenthal. "Iron-mediated cardiovascular injury." Vascular Medicine 4, no. 2 (May 1999): 93–99. http://dx.doi.org/10.1177/1358836x9900400207.

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Iron is an essential element for normal cellular function and general health. However, iron may play a pathologic role in certain cardiac conditions including reperfusion injury, hemochromatosis, b-thalassemia and coronary atherosclerosis. It also may play a role in injury due to anthracycline cardiotoxicity. Removal of iron via phlebotomy for hemochromatosis and chelation therapy for b-thalassemia are proven treatments. Cell culture, and isolated organ and animal studies suggest that depleting iron stores may prevent reperfusion injury, restenosis and even atherogenesis. This article will review mechanisms by which iron overload states and normal iron stores contribute to cardiovascular pathophysiology and the accumulating evidence that iron chelation may prevent restenosis and atherogenesis.

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28

Orellana-Urzúa, Sofía, Ignacio Rojas, Lucas Líbano, and Ramón Rodrigo. "Pathophysiology of Ischemic Stroke: Role of Oxidative Stress." Current Pharmaceutical Design 26, no. 34 (October 13, 2020): 4246–60. http://dx.doi.org/10.2174/1381612826666200708133912.

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Stroke is the second leading cause of mortality and the major cause of adult physical disability worldwide. The currently available treatment to recanalize the blood flow in acute ischemic stroke is intravenous administration of tissue plasminogen activator (t-PA) and endovascular treatment. Nevertheless, those treatments have the disadvantage that reperfusion leads to a highly harmful reactive oxygen species (ROS) production, generating oxidative stress (OS), which is responsible for most of the ischemia-reperfusion injury and thus causing brain tissue damage. In addition, OS can lead brain cells to apoptosis, autophagy and necrosis. The aims of this review are to provide an updated overview of the role of OS in brain IRI, providing some bases for therapeutic interventions based on counteracting the OS-related mechanism of injury and thus suggesting novel possible strategies in the prevention of IRI after stroke.

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29

Montalvo-Jave, Eduardo E., Tomas Escalante-Tattersfield, Jose A. Ortega-Salgado, Enrique Piña, and David A. Geller. "Factors in the Pathophysiology of the Liver Ischemia-Reperfusion Injury." Journal of Surgical Research 147, no. 1 (June 2008): 153–59. http://dx.doi.org/10.1016/j.jss.2007.06.015.

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30

Welbourn, C. R. B., G. Goldman, I. S. Paterson, C. R. Valeri, D. Shepro, and H. B. Hechtman. "Pathophysiology of ischaemia reperfusion injury: Central role of the neutrophil." British Journal of Surgery 78, no. 6 (June 1991): 651–55. http://dx.doi.org/10.1002/bjs.1800780607.

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31

Rossello, Xavier, Manuel Lobo-Gonzalez, and Borja Ibanez. "Editor’s Choice- Pathophysiology and therapy of myocardial ischaemia/reperfusion syndrome." European Heart Journal: Acute Cardiovascular Care 8, no. 5 (June 7, 2019): 443–56. http://dx.doi.org/10.1177/2048872619845283.

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There is a need to find interventions able to reduce the extent of injury in reperfused ST-segment elevation myocardial infarction (STEMI) beyond timely reperfusion. In this review, we summarise the clinical impact of STEMI from epidemiological, clinical and biological perspectives. We also revise the pathophysiology underlying the ischaemia/reperfusion syndrome occurring in reperfused STEMI, including the several players involved in this syndrome, such as cardiomyocytes, microcirculation and circulating cells. Interventions aimed to reduce the resultant infarct size, known as cardioprotective therapies, are extensively discussed, putting the focus on both mechanical interventions (i.e. ischaemic conditioning) and promising pharmacological therapies, such as early intravenous metoprolol, exenatide and other glucose modulators, N-acetylcysteine as well as on some other classic therapies which have failed to be translated to the clinical arena. Novel targets for evolving therapeutic interventions to ameliorate ischaemia/reperfusion injury are also discussed. Finally, we highlight the necessity to improve the study design of future randomised clinical trials in the field, as well as to select patients better who can most likely benefit from cardioprotective interventions.

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32

Ferrari, Renata Salatti, and Cristiano Feijó Andrade. "Oxidative Stress and Lung Ischemia-Reperfusion Injury." Oxidative Medicine and Cellular Longevity 2015 (2015): 1–14. http://dx.doi.org/10.1155/2015/590987.

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Ischemia-reperfusion (IR) injury is directly related to the formation of reactive oxygen species (ROS), endothelial cell injury, increased vascular permeability, and the activation of neutrophils and platelets, cytokines, and the complement system. Several studies have confirmed the destructiveness of the toxic oxygen metabolites produced and their role in the pathophysiology of different processes, such as oxygen poisoning, inflammation, and ischemic injury. Due to the different degrees of tissue damage resulting from the process of ischemia and subsequent reperfusion, several studies in animal models have focused on the prevention of IR injury and methods of lung protection. Lung IR injury has clinical relevance in the setting of lung transplantation and cardiopulmonary bypass, for which the consequences of IR injury may be devastating in critically ill patients.

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33

de Holanda, Gustavo Sampaio, Samuel dos Santos Valença, Amabile Maran Carra, Renata Cristina Lopes Lichtenberger, Bianca de Castilho, Olavo Borges Franco, João Alfredo de Moraes, and Alberto Schanaider. "Translational Application of Fluorescent Molecular Probes for the Detection of Reactive Oxygen and Nitrogen Species Associated with Intestinal Reperfusion Injury." Metabolites 11, no. 12 (November 26, 2021): 802. http://dx.doi.org/10.3390/metabo11120802.

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Acute mesenteric ischemia, caused by an abrupt interruption of blood flow in the mesenteric vessels, is associated with high mortality. When treated with surgical interventions or drugs to re-open the vascular lumen, the reperfusion process itself can inflict damage to the intestinal wall. Ischemia and reperfusion injury comprise complex mechanisms involving disarrangement of the splanchnic microcirculatory flow and impairment of the mitochondrial respiratory chain due to initial hypoxemia and subsequent oxidative stress during the reperfusion phase. This pathophysiologic process results in the production of large amounts of reactive oxygen (ROS) and nitrogen (RNS) species, which damage deoxyribonucleic acid, protein, lipids, and carbohydrates by autophagy, mitoptosis, necrosis, necroptosis, and apoptosis. Fluorescence-based systems using molecular probes have emerged as highly effective tools to monitor the concentrations and locations of these often short-lived ROS and RNS. The timely and accurate detection of both ROS and RNS by such an approach would help to identify early injury events associated with ischemia and reperfusion and increase overall clinical diagnostic sensitivity. This abstract describes the pathophysiology of intestinal ischemia and reperfusion and the early biological laboratory diagnosis using fluorescent molecular probes anticipating clinical decisions in the face of an extremely morbid disease.

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34

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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35

Schwarzer, Michael, Susanne Rohrbach, and Bernd Niemann. "Heart and Mitochondria: Pathophysiology and Implications for Cardiac Surgeons." Thoracic and Cardiovascular Surgeon 66, no. 01 (December 19, 2017): 011–19. http://dx.doi.org/10.1055/s-0037-1615263.

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Excluding the heart from systemic circulation during cardiac surgery renders the myocardium ischemic, resulting in cardiac damage. In addition, another hit to the myocardium will occur upon restoration of blood flow, in the reperfusion phase. Experimental data from animal models have revealed that loss of cardiac metabolic flexibility and mitochondrial dysfunctions contributes to contractile impairment in hypertrophied, failing, obese, and diabetic hearts. Such diseased hearts are prone to myocardial ischemia–reperfusion (I/R) injury. Although analyses in human cardiac samples are not as comprehensive as animal data, similar disease-associated metabolic and mitochondrial changes exist. Considering increasing age and comorbidities in patients nowadays, it is not surprising that I/R injuries remain a major cause of morbidity and mortality after cardiac surgery. Mitochondria have emerged as critical targets but also key regulators of myocardial I/R injury, and the extent of mitochondrial damage is a major determinant of myocardial I/R injury. Although cardioprotective mechanisms are diverse, many come together and involve steps at the point of mitochondria. We will, therefore, provide a description of mitochondrial alterations observed in various cardiac disease states and discuss the current experimental knowledge of the role of mitochondria in I/R and of potential protective mechanisms against myocardial I/R injury involving mitochondria. Within this review, we will focus on the protection against I/R injury conferred by caloric restriction (CR) and by ischemic conditioning. Further research is needed to establish whether strategies targeting mitochondria, which have been proposed from preclinical studies, could be translated into cardioprotective therapies against I/R injury in patients.

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36

Imran, Rajeel, Ghada A. Mohamed, and Fadi Nahab. "Acute Reperfusion Therapies for Acute Ischemic Stroke." Journal of Clinical Medicine 10, no. 16 (August 19, 2021): 3677. http://dx.doi.org/10.3390/jcm10163677.

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The field of acute stroke treatment has made tremendous progress in reducing the overall burden of disability. Understanding the pathophysiology of acute ischemic injury, neuroimaging to quantify the extent of penumbra and infarction, and acute stroke reperfusion therapies have together contributed to these advancements. In this review we highlight advancements in reperfusion therapies for acute ischemic stroke.

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37

Cooper, DeLinda Jo. "Induced Hypothermia for Neonatal Hypoxic-Ischemic Encephalopathy: Pathophysiology, Current Treatment, and Nursing Considerations." Neonatal Network 30, no. 1 (2011): 29–36. http://dx.doi.org/10.1891/0730-0832.30.1.29.

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AbstractHypoxic-ischemic encephalopathy (HIE) can lead to devastating neurodevelopmental consequences such as cerebral palsy, seizure disorders, and significant developmental delays. HIE in the newborn is often the result of a hypoxic event, such as uterine rupture, placental abruption, or cord prolapse. Biphasic brain injury occurs in HIE. The first phase involves activation of the sympathetic nervous system as a compensatory mechanism. The second phase, known as reperfusion brain injury, occurs hours later. Induced hypothermia, a neuroprotective strategy for treating HIE, targets the second phase to prevent reperfusion injury. NICU nurses are in a unique position to detect patient instability and to maintain the therapeutic interventions that contribute to the healing process. This article highlights the significant role nurses play in the management of infants diagnosed with HIE who are treated with induced hypothermia.

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Neri, Margherita, Irene Riezzo, Natascha Pascale, Cristoforo Pomara, and Emanuela Turillazzi. "Ischemia/Reperfusion Injury following Acute Myocardial Infarction: A Critical Issue for Clinicians and Forensic Pathologists." Mediators of Inflammation 2017 (2017): 1–14. http://dx.doi.org/10.1155/2017/7018393.

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Acute myocardial infarction (AMI) is a leading cause of morbidity and mortality. Reperfusion strategies are the current standard therapy for AMI. However, they may result in paradoxical cardiomyocyte dysfunction, known as ischemic reperfusion injury (IRI). Different forms of IRI are recognized, of which only the first two are reversible: reperfusion-induced arrhythmias, myocardial stunning, microvascular obstruction, and lethal myocardial reperfusion injury. Sudden death is the most common pattern for ischemia-induced lethal ventricular arrhythmias during AMI. The exact mechanisms of IRI are not fully known. Molecular, cellular, and tissue alterations such as cell death, inflammation, neurohumoral activation, and oxidative stress are considered to be of paramount importance in IRI. However, comprehension of the exact pathophysiological mechanisms remains a challenge for clinicians. Furthermore, myocardial IRI is a critical issue also for forensic pathologists since sudden death may occur despite timely reperfusion following AMI, that is one of the most frequently litigated areas of cardiology practice. In this paper we explore the literature regarding the pathophysiology of myocardial IRI, focusing on the possible role of the calpain system, oxidative-nitrosative stress, and matrix metalloproteinases and aiming to foster knowledge of IRI pathophysiology also in terms of medicolegal understanding of sudden deaths following AMI.

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Chen-Yoshikawa, Toyofumi Fengshi. "Ischemia–Reperfusion Injury in Lung Transplantation." Cells 10, no. 6 (May 28, 2021): 1333. http://dx.doi.org/10.3390/cells10061333.

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Lung transplantation has been established worldwide as the last treatment for end-stage respiratory failure. However, ischemia–reperfusion injury (IRI) inevitably occurs after lung transplantation. The most severe form of IRI leads to primary graft failure, which is an important cause of morbidity and mortality after lung transplantation. IRI may also induce rejection, which is the main cause of mortality in recipients. Despite advances in donor management and graft preservation, most donor grafts are still unsuitable for transplantation. Although the pulmonary endothelium is the primary target site of IRI, the pathophysiology of lung IRI remains incompletely understood. It is essential to understand the mechanism of pulmonary IRI to improve the outcomes of lung transplantation. Therefore, we reviewed the state-of-the-art in the management of pulmonary IRI after lung transplantation. Recently, the ex vivo lung perfusion (EVLP) system has been clinically introduced worldwide. Various promising therapeutic strategies for the protection of the endothelium against IRI, including EVLP, inhalation therapy with therapeutic gases and substances, fibrinolytic treatment, and mesenchymal stromal cell therapy, are awaiting clinical application. We herein review the latest advances in the field of pulmonary IRI in lung transplantation.

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Kudaibergenova, Assel, Nurettin Aydogdu, Nihayet Kandemir, and Muhammed Ali Aydin. "Investigation of Kisspeptin Role in Experimental Kidney Ischemia/Reperfusion Injury." Folia Medica 62, no. 1 (March 31, 2020): 82–88. http://dx.doi.org/10.3897/folmed.62.e47913.

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Introduction: Kisspeptin is biologically active peptide encoded by the KISS1 gene that is structurally found in the kidney tubule, collecting duct and vein smooth muscle cells.    Aim: We aimed to investigate the role of kisspeptin in kidney function and renal pathophysiology in experimental kidney ischemia/reperfusion (I/R) injury.    Materials and methods: Male Spraque-Dawley rats were divided into control and I/R groups (n=8). Both kidney vessels of I/R group rats were clamped and subjected to ischemia for 60 minutes and reperfusion for 48 hours. After the reperfusion period blood samples and kidney tissue were collected under anesthesia.    Results: Levels of urea, creatinine (p<0.01) in serum, Kim-1 in urine (p<0.05) were increased, creatinine clearance, aldosterone and ANG II levels in serum were decreased in the I/R group compared with the Control group (p<0.05). Kidney kisspeptin levels decreased and urine kisspeptin levels increased (p<0.05).    Conclusions: The present study has shown that the levels of kisspeptin change in kidney damage and thus the kisspeptin may play a role in the regulation of renal function and in the pathophysiology of acute kidney injury.

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Zhao, Zhuo, Wei Sun, Ziyuan Guo, Bin Liu, Hongyu Yu, and Jichang Zhang. "Long Noncoding RNAs in Myocardial Ischemia-Reperfusion Injury." Oxidative Medicine and Cellular Longevity 2021 (April 5, 2021): 1–15. http://dx.doi.org/10.1155/2021/8889123.

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Following an acute myocardial infarction, reperfusion therapy is currently the most effective way to save the ischemic myocardium; however, restoring blood flow may lead to a myocardial ischemia-reperfusion injury (MIRI). Recent studies have confirmed that long-chain noncoding RNAs (LncRNAs) play important roles in the pathophysiology of MIRIs. These LncRNA-mediated roles include cardiomyocyte apoptosis, autophagy, necrosis, oxidative stress, inflammation, mitochondrial dysfunction, and calcium overload, which are regulated through the expression of target genes. Thus, LncRNAs may be used as clinical diagnostic markers and therapeutic targets to treat or prevent MIRI. This review evaluates the research on LncRNAs involved in MIRIs and provides new ideas for preventing and treating this type of injury.

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Sánchez-Hernández, César Daniel, Lucero Aidé Torres-Alarcón, Ariadna González-Cortés, and Alberto N. Peón. "Ischemia/Reperfusion Injury: Pathophysiology, Current Clinical Management, and Potential Preventive Approaches." Mediators of Inflammation 2020 (January 29, 2020): 1–13. http://dx.doi.org/10.1155/2020/8405370.

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Myocardial ischemia reperfusion syndrome is a complex entity where many inflammatory mediators play different roles, both to enhance myocardial infarction-derived damage and to heal injury. In such a setting, the establishment of an effective therapy to treat this condition has been elusive, perhaps because the experimental treatments have been conceived to block just one of the many pathogenic pathways of the disease, or because they thwart the tissue-repairing phase of the syndrome. Either way, we think that a discussion about the pathophysiology of the disease and the mechanisms of action of some drugs may shed some clarity on the topic.

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Jaeschke, Hartmut. "Pathophysiology of hepatic ischemia-reperfusion injury: The role of complement activation." Gastroenterology 107, no. 2 (August 1994): 583–86. http://dx.doi.org/10.1016/0016-5085(94)90188-0.

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Pan, Jie, Angelos-Aristeidis Konstas, Brian Bateman, Girolamo A. Ortolano, and John Pile-Spellman. "Reperfusion injury following cerebral ischemia: pathophysiology, MR imaging, and potential therapies." Neuroradiology 49, no. 2 (December 20, 2006): 93–102. http://dx.doi.org/10.1007/s00234-006-0183-z.

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Saeid, Feyzizadeh, Javadi Aniseh, Badalzadeh Reza, and Vafaee S. Manouchehr. "Signaling mediators modulated by cardioprotective interventions in healthy and diabetic myocardium with ischaemia–reperfusion injury." European Journal of Preventive Cardiology 25, no. 14 (February 14, 2018): 1463–81. http://dx.doi.org/10.1177/2047487318756420.

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Ischaemic heart diseases are one of the major causes of death in the world. In most patients, ischaemic heart disease is coincident with other risk factors such as diabetes. Patients with diabetes are more prone to cardiac ischaemic dysfunctions including ischaemia–reperfusion injury. Ischaemic preconditioning, postconditioning and remote conditionings are reliable interventions to protect the myocardium against ischaemia–reperfusion injuries through activating various signaling pathways and intracellular mediators. Diabetes can disrupt the intracellular signaling cascades involved in these myocardial protections, and studies have revealed that cardioprotective effects of the conditioning interventions are diminished in the diabetic condition. The complex pathophysiology and poor prognosis of ischaemic heart disease among people with diabetes necessitate the investigation of the interaction of diabetes with ischaemia–reperfusion injury and cardioprotective mechanisms. Reducing the outcomes of ischaemia–reperfusion injury using targeted strategies would be particularly helpful in this population. In this study, we review the protective interventional signaling pathways and mediators which are activated by ischaemic conditioning strategies in healthy and diabetic myocardium with ischaemia–reperfusion injury.

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Gracia-Sancho, Jordi, Araní Casillas-Ramírez, and Carmen Peralta. "Molecular pathways in protecting the liver from ischaemia/reperfusion injury: a 2015 update." Clinical Science 129, no. 4 (May 21, 2015): 345–62. http://dx.doi.org/10.1042/cs20150223.

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Ischaemia/reperfusion injury is an important cause of liver damage during surgical procedures such as hepatic resection and liver transplantation, and represents the main cause of graft dysfunction post-transplantation. Molecular processes occurring during hepatic ischaemia/reperfusion are diverse, and continuously include new and complex mechanisms. The present review aims to summarize the newest concepts and hypotheses regarding the pathophysiology of liver ischaemia/reperfusion, making clear distinction between situations of cold and warm ischaemia. Moreover, the most updated therapeutic strategies including pharmacological, genetic and surgical interventions, as well as some of the scientific controversies in the field are described.

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Tang, Jinhua, and Shougang Zhuang. "Histone acetylation and DNA methylation in ischemia/reperfusion injury." Clinical Science 133, no. 4 (February 2019): 597–609. http://dx.doi.org/10.1042/cs20180465.

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Abstract Ischemic/reperfusion (I/R) injury causes a series of serious clinical problems associated with high morbidity and mortality in various disorders, such as acute kidney injury (AKI), myocardial infarction, ischemic stroke, circulatory arrest, and peripheral vascular disease. The pathophysiology and pathogenesis of I/R injury is complex and multifactorial. Recent studies have revealed that epigenetic regulation is critically involved in the pathogenesis of I/R-induced tissue injury. In this review, we will sum up recent advances on the modification, regulation, and implication of histone modifications and DNA methylation in I/R injury-induced organ dysfunction. Understandings of I/R-induced epigenetic alterations and regulations will aid in the development of potential therapeutics.

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Jaeschke, Hartmut. "Molecular mechanisms of hepatic ischemia-reperfusion injury and preconditioning." American Journal of Physiology-Gastrointestinal and Liver Physiology 284, no. 1 (January 1, 2003): G15—G26. http://dx.doi.org/10.1152/ajpgi.00342.2002.

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Ischemia-reperfusion injury is, at least in part, responsible for the morbidity associated with liver surgery under total vascular exclusion or after liver transplantation. The pathophysiology of hepatic ischemia-reperfusion includes a number of mechanisms that contribute to various degrees in the overall injury. Some of the topics discussed in this review include cellular mechanisms of injury, formation of pro- and anti-inflammatory mediators, expression of adhesion molecules, and the role of oxidant stress during the inflammatory response. Furthermore, the roles of nitric oxide in preventing microcirculatory disturbances and as a substrate for peroxynitrite formation are reviewed. In addition, emerging mechanisms of protection by ischemic preconditioning are discussed. On the basis of current knowledge, preconditioning or pharmacological interventions that mimic these effects have the greatest potential to improve clinical outcome in liver surgery involving ischemic stress and reperfusion.

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Nieuwenhuijs-Moeke, Gertrude J., Søren E. Pischke, Stefan P. Berger, Jan Stephan F. Sanders, Robert A. Pol, Michel M. R. F. Struys, Rutger J. Ploeg, and Henri G. D. Leuvenink. "Ischemia and Reperfusion Injury in Kidney Transplantation: Relevant Mechanisms in Injury and Repair." Journal of Clinical Medicine 9, no. 1 (January 17, 2020): 253. http://dx.doi.org/10.3390/jcm9010253.

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Ischemia and reperfusion injury (IRI) is a complex pathophysiological phenomenon, inevitable in kidney transplantation and one of the most important mechanisms for non- or delayed function immediately after transplantation. Long term, it is associated with acute rejection and chronic graft dysfunction due to interstitial fibrosis and tubular atrophy. Recently, more insight has been gained in the underlying molecular pathways and signalling cascades involved, which opens the door to new therapeutic opportunities aiming to reduce IRI and improve graft survival. This review systemically discusses the specific molecular pathways involved in the pathophysiology of IRI and highlights new therapeutic strategies targeting these pathways.

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Panisello-Roselló, Arnau, Joan Roselló-Catafau, and René Adam. "New Insights in Molecular Mechanisms and Pathophysiology of Ischemia-Reperfusion Injury 2.0: An Updated Overview." International Journal of Molecular Sciences 22, no. 1 (December 22, 2020): 28. http://dx.doi.org/10.3390/ijms22010028.

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