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Journal articles on the topic 'Ischemia – Pathophysiology'

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Published: 4 June 2021
Last updated: 21 February 2023

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1

Siesjö, Bo K. "Pathophysiology and treatment of focal cerebral ischemia." Journal of Neurosurgery 77, no. 3 (September 1992): 337–54. http://dx.doi.org/10.3171/jns.1992.77.3.0337.

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✓ The mechanisms that give rise to ischemic brain damage have not been definitively determined, but considerable evidence exists that three major factors are involved: increases in the intercellular cytosolic calcium concentration (Ca++i), acidosis, and production of free radicals. A nonphysiological rise in Ca++i due to a disturbed pump/leak relationship for calcium is believed to cause cell damage by overactivation of lipases and proteases and possibly also of endonucleases, and by alterations of protein phosphorylation, which secondarily affects protein synthesis and genome expression. The severity of this disturbance depends on the density of ischemia. In complete or near-complete ischemia of the cardiac arrest type, pump activity has ceased and the calcium leak is enhanced by the massive release of excitatory amino acids. As a result, multiple calcium channels are opened. This is probably the scenario in the focus of an ischemic lesion due to middle cerebral artery occlusion. Such ischemic tissues can be salvaged only by recirculation, and any brain damage incurred is delayed, suggesting that the calcium transient gives rise to sustained changes in membrane function and metabolism. If the ischemia is less dense, as in the penumbral zone of a focal ischemic lesion, pump failure may be moderate and the leak may be only slightly or intermittently enhanced. These differences in the pump/leak relationship for calcium explain why calcium and glutamate antagonists may lack effect on the cardiac arrest type of ischemia, while decreasing infarct size in focal ischemia. The adverse effects of acidosis may be exerted by several mechanisms. When the ischemia is sustained, acidosis may promote edema formation by inducing Na+ and Cl− accumulation via coupled Na+/H+ and Cl−/HCO3− exchange; however, it may also prevent recovery of mitochondrial metabolism and resumption of H+ extrusion. If the ischemia is transient, pronounced intraischemic acidosis triggers delayed damage characterized by gross edema and seizures. Possibly, this is a result of free-radical formation. If the ischemia is moderate, as in the penumbral zone of a focal ischemic lesion, the effect of acidosis is controversial. In fact, enhanced glucolysis may then be beneficial. Although free radicals have long been assumed to be mediators of ischemic cell death, it is only recently that more substantial evidence of their participation has been produced. It now seems likely that one major target of free radicals is the microvasculature, and that free radicals and other mediators of inflammatory reactions (such as platelet-activating factor) aggravate the ischemic lesion by causing microvascular dysfunction and blood-brain barrier disruption. Solid experimental evidence exists that the infarct resulting from middle cerebral artery occlusion can be reduced by glutamate antagonists, by several calcium antagonists, and by some drugs acting on Ca++ and Na+ influx. In addition, published reports hint that qualitatively similar results are obtained with drugs whose sole or main effect is to scavenge free radicals. Thus, there is substantial experimental evidence that the ischemic lesions due to middle cerebral artery occlusion can be ameliorated by drugs, sometimes dramatically; however, the therapeutic window seems small, maximally 3 to 6 hours. This suggests that if these therapeutic principles are to be successfully applied to the clinical situation, patient management must change.
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2

Siesjö, Bo K. "Pathophysiology and treatment of focal cerebral ischemia." Journal of Neurosurgery 108, no. 3 (March 2008): 616–31. http://dx.doi.org/10.3171/jns/2008/108/3/0616.

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✓ This article examines the pathophysiology of lesions caused by focal cerebral ischemia. Ischemia due to middle cerebral artery occlusion encompasses a densely ischemic focus and a less densely ischemic penumbral zone. Cells in the focus are usually doomed unless reperfusion is quickly instituted. In contrast, although the penumbra contains cells “at risk,” these may remain viable for at least 4 to 8 hours. Cells in the penumbra may be salvaged by reperfusion or by drugs that prevent an extension of the infarction into the penumbral zone. Factors responsible for such an extension probably include acidosis, edema, K+/Ca++ transients, and inhibition of protein synthesis. Central to any discussion of the pathophysiology of ischemic lesions is energy depletion. This is because failure to maintain cellular adenosine triphosphate (ATP) levels leads to degradation of macromolecules of key importance to membrane and cytoskeletal integrity, to loss of ion homeostasis, involving cellular accumulation of Ca++, Na+, and Cl−, with osmotically obligated water, and to production of metabolic acids with a resulting decrease in intra- and extracellular pH. In all probability, loss of cellular calcium homeostasis plays an important role in the pathogenesis of ischemic cell damage. The resulting rise in the free cytosolic intracellular calcium concentration (Ca++) depends on both the loss of calcium pump function (due to ATP depletion), and the rise in membrane permeability to calcium. In ischemia, calcium influx occurs via multiple pathways. Some of the most important routes depend on activation of receptors by glutamate and associated excitatory amino acids released from depolarized presynaptic endings. However, ischemia also interferes with the intracellular sequestration and binding of calcium, thereby contributing to the rise in intracellular Ca++. A second key event in the ischemic tissue is activation of anaerobic glucolysis. The main reason for this activation is inhibition of mitochondrial metabolism by lack of oxygen; however, other factors probably contribute. For example, there is a complex interplay between loss of cellular calcium homeostasis and acidosis. On the one hand, a rise in intracellular Ca++ is apt to cause mitochondrial accumulation of calcium. This must interfere with ATP production and enhance anaerobic glucolysis. On the other hand, acidosis must interfere with calcium binding, thereby contributing to the rise in intracellular Ca++.
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3

Siesjö, Bo K. "Pathophysiology and treatment of focal cerebral ischemia." Journal of Neurosurgery 77, no. 2 (August 1992): 169–84. http://dx.doi.org/10.3171/jns.1992.77.2.0169.

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✓ This article examines the pathophysiology of lesions caused by focal cerebral ischemia. Ischemia due to middle cerebral artery occlusion encompasses a densely ischemic focus and a less densely ischemic penumbral zone. Cells in the focus are usually doomed unless reperfusion is quickly instituted. In contrast, although the penumbra contains cells “at risk.” these may remain viable for at least 4 to 8 hours. Cells in the penumbra may be salvaged by reperfusion or by drugs that prevent an extension of the infarction into the penumbral zone. Factors responsible for such an extension probably include acidosis, edema, K+/Ca++ transients, and inhibition of protein synthesis. Central to any discussion of the pathophysiology of ischemic lesions is energy depletion. This is because failure to maintain cellular adenosine triphosphate (ATP) levels leads to degradation of macromolecules of key importance to membrane and cytoskeletal integrity, to loss of ion homeostasis, involving cellular accumulation of Ca++, Na+, and Cl−, with osmotically obligated water, and to production of metabolic acids with a resulting decrease in intra- and extracellular pH. In all probability, loss of cellular calcium homeostasis plays an important role in the pathogenesis of ischemic cell damage. The resulting rise in the free cytosolic intracellular calcium concentration (Ca++) depends on both the loss of calcium pump function (due to ATP depletion), and the rise in membrane permeability to calcium. In ischemia, calcium influx occurs via multiple pathways. Some of the most important routes depend on activation of receptors by glutamate and associated excitatory amino acids released from depolarized presynaptic endings. However, ischemia also interferes with the intracellular sequestration and binding of calcium, thereby contributing to the rise in intracellular Ca++. A second key event in the ischemic tissue is activation of anaerobic glucolysis. The main reason for this activation is inhibition of mitochondrial metabolism by lack of oxygen; however, other factors probably contribute. For example, there is a complex interplay between loss of cellular calcium homeostasis and acidosis. On the one hand, a rise in intracellular Ca++ is apt to cause mitochondrial accumulation of calcium. This must interfere with ATP production and enhance anaerobic glucolysis. On the other hand, acidosis must interfere with calcium binding, thereby contributing to the rise in intracellular Ca++.
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4

MACDONALD, R. Loch, and Marcus STOODLEY. "Pathophysiology of Cerebral Ischemia." Neurologia medico-chirurgica 38, no. 1 (1998): 1–11. http://dx.doi.org/10.2176/nmc.38.1.

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5

Patel, Amit, Ronald N. Kaleya, and Robert J. Sammartano. "Pathophysiology of Mesenteric Ischemia." Surgical Clinics of North America 72, no. 1 (February 1992): 31–41. http://dx.doi.org/10.1016/s0039-6109(16)45626-4.

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6

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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7

Tran, T. P., R. Muelleman, I. Pipinos, M. Watkins, and H. Albadawi. "Ischemic Mitochondriopathy in the Pathophysiology of Ischemia/Reperfusion Syndrome." Journal of Emergency Medicine 33, no. 3 (October 2007): 337. http://dx.doi.org/10.1016/j.jemermed.2007.08.045.

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8

Severino, Paolo, Andrea D’Amato, Lucrezia Netti, Mariateresa Pucci, Fabio Infusino, Viviana Maestrini, Massimo Mancone, and Francesco Fedele. "Myocardial Ischemia and Diabetes Mellitus: Role of Oxidative Stress in the Connection between Cardiac Metabolism and Coronary Blood Flow." Journal of Diabetes Research 2019 (April 4, 2019): 1–16. http://dx.doi.org/10.1155/2019/9489826.

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Ischemic heart disease (IHD) has several risk factors, among which diabetes mellitus represents one of the most important. In diabetic patients, the pathophysiology of myocardial ischemia remains unclear yet: some have atherosclerotic plaque which obstructs coronary blood flow, others show myocardial ischemia due to coronary microvascular dysfunction in the absence of plaques in epicardial vessels. In the cross-talk between myocardial metabolism and coronary blood flow (CBF), ion channels have a main role, and, in diabetic patients, they are involved in the pathophysiology of IHD. The exposition to the different cardiovascular risk factors and the ischemic condition determine an imbalance of the redox state, defined as oxidative stress, which shows itself with oxidant accumulation and antioxidant deficiency. In particular, several products of myocardial metabolism, belonging to oxidative stress, may influence ion channel function, altering their capacity to modulate CBF, in response to myocardial metabolism, and predisposing to myocardial ischemia. For this reason, considering the role of oxidative and ion channels in the pathophysiology of myocardial ischemia, it is allowed to consider new therapeutic perspectives in the treatment of IHD.
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9

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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10

Simon, F., A. Oberhuber, N. Floros, P. Düppers, H. Schelzig, and M. Duran. "Pathophysiology of chronic limb ischemia." Gefässchirurgie 23, S1 (April 10, 2018): 13–18. http://dx.doi.org/10.1007/s00772-018-0380-1.

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11

Foreman, Brandon. "The Pathophysiology of Delayed Cerebral Ischemia." Journal of Clinical Neurophysiology 33, no. 3 (June 2016): 174–82. http://dx.doi.org/10.1097/wnp.0000000000000273.

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12

Cox, D. P. M. "CEREBRAL ISCHEMIA: MOLECULAR AND CELLULAR PATHOPHYSIOLOGY." Brain 123, no. 4 (April 1, 2000): 847–48. http://dx.doi.org/10.1093/brain/123.4.847.

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13

Zwolak, Robert, and John M. Porter. "Intestinal ischemia disorders: pathophysiology and management." Journal of Vascular Surgery 30, no. 4 (October 1999): A1. http://dx.doi.org/10.1016/s0741-5214(99)70128-x.

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14

Sidawy, Anton N. "Intestinal Ischemia Disorders: Pathophysiology and Management." Annals of Vascular Surgery 13, no. 5 (September 1999): 550. http://dx.doi.org/10.1016/s0890-5096(06)61810-4.

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15

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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16

Knopes, Keith D., John B. Leslie, and Martin J. London. "Pathophysiology and treatment of myocardial ischemia." Journal of Cardiothoracic Anesthesia 4, no. 5 (October 1990): 51–54. http://dx.doi.org/10.1016/s0888-6296(11)80011-6.

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17

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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18

Mondy III, J. S. "Intestinal Ischemia Disorders: Pathophysiology and Management." Archives of Surgery 134, no. 8 (August 1, 1999): 899–900. http://dx.doi.org/10.1001/archsurg.134.8.899.

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19

Bramlett, Helen M., and W. Dalton Dietrich. "Pathophysiology of Cerebral Ischemia and Brain Trauma: Similarities and Differences." Journal of Cerebral Blood Flow & Metabolism 24, no. 2 (February 2004): 133–50. http://dx.doi.org/10.1097/01.wcb.0000111614.19196.04.

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Current knowledge regarding the pathophysiology of cerebral ischemia and brain trauma indicates that similar mechanisms contribute to loss of cellular integrity and tissue destruction. Mechanisms of cell damage include excitotoxicity, oxidative stress, free radical production, apoptosis and inflammation. Genetic and gender factors have also been shown to be important mediators of pathomechanisms present in both injury settings. However, the fact that these injuries arise from different types of primary insults leads to diverse cellular vulnerability patterns as well as a spectrum of injury processes. Blunt head trauma produces shear forces that result in primary membrane damage to neuronal cell bodies, white matter structures and vascular beds as well as secondary injury mechanisms. Severe cerebral ischemic insults lead to metabolic stress, ionic perturbations, and a complex cascade of biochemical and molecular events ultimately causing neuronal death. Similarities in the pathogenesis of these cerebral injuries may indicate that therapeutic strategies protective following ischemia may also be beneficial after trauma. This review summarizes and contrasts injury mechanisms after ischemia and trauma and discusses neuroprotective strategies that target both types of injuries.
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20

Liu, Yuezhu, Hua Zeng, and Junmei Xu. "Recent Advance on Drug Therapy Related to Myocardial Ischemia Reperfusion Injury." Journal of Biomaterials and Tissue Engineering 12, no. 2 (February 1, 2022): 299–305. http://dx.doi.org/10.1166/jbt.2022.2899.

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Myocardial ischemia reperfusion injury (MIRI) means complete or partial artery obstruction of coronary artery, and ischemic myocardium will be recirculating in a period of time. Although the ischemic myocardium can be restored to normal perfusion, its tissue damage will instead be progressive. An aggravated pathological process. MIRI is a complex entity where many inflammatory mediators play different roles, both to enhance myocardial infarction-derived damage and to heal injury. Therefore, the research and development of drugs for the prevention and treatment of this period has also become the focus. This article first studied pathophysiology of MIRI, and reviewed the research progress of MIRI-related drugs. Research results show that: MIRI is inevitable for myocardial ischemia, with the possible to double damage via the ischemic condition. Therefore, it is a serious complication and one of the most popular diseases in the world. It has always been difficult to find an effective treatment for this disease, because it is difficult to explore the inflammation behind its pathophysiology.
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21

Sandstrom, Claire. "Pathophysiology and Imaging Diagnosis of Acute Mesenteric Ischemia." Digestive Disease Interventions 02, no. 03 (August 7, 2018): 195–209. http://dx.doi.org/10.1055/s-0038-1667344.

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AbstractAcute mesenteric ischemia is a potentially life-threatening condition associated with high mortality, particularly with any delay in treatment. Prompt diagnosis with imaging is crucial to achieve a favorable outcome. Both arterial and venous etiologies can result in ischemia, and the radiologist plays a central role in the initial evaluation of a patient with suspected acute mesenteric ischemia to guide management decisions. This article will review the appropriate imaging evaluation of a patient with suspected acute mesenteric ischemia. The overlapping and the distinguishing findings on imaging, as well as the relevant clinical features, will be discussed for the spectrum of both common and uncommon etiologies of mesenteric ischemia.
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22

Blaisdell, F. William. "The Pathophysiology of Skeletal Muscle Ischemia and the Reperfusion Syndrome: A Review." Cardiovascular Surgery 10, no. 6 (December 2002): 620–30. http://dx.doi.org/10.1177/096721090201000620.

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There are two components to the reperfusion syndrome, which follows extremity ischemia. The local response, which follows reperfusion. consists of limb swelling with its potential for aggravating tissue injury and the systemic response, which results in multiple organ failure and death. It is apparent that skeletal muscle is the predominant tissue in the limb but also the tissue that is most vulnerable to ischemia. Physiological and anatomical studies show that irreversible muscle cell damage starts after 3 h of ischemia and is nearly complete at 6 h. These muscle changes are paralleled by progressive microvascular damage. Microvascular changes appear to follow rather than precede skeletal muscle damage as the tolerance of capillaries to ischemia vary with the tissue being reperfused. The more severe the cellular damage the greater the microvascular changes and with death of tissue microvascular flow ceases within a few hours—the no reflow phenomenon. At this point tissue swelling ceases. The inflammatory responses following reperfusion varies greatly. When muscle tissue death is uniform, as would follow tourniquet ischemia or limb replantation, little inflammatory response results. In most instances of reperfusion, which follows thrombotic or embolic occlusion, there will be a variable degree of ischemic damage in the zone where collateral blood flow is possible. The extent of this region will determine the magnitude of the inflammatory response, whether local or systemic. Only in this region will therapy be of any benefit, whether fasciotomy to prevent pressure occlusion of the microcirculation, or anticoagulation to prevent further microvascular thrombosis. Since many of the inflammatory mediators are generated by the act of clotting, anticoagulation will have additional benefit by decreasing the inflammatory response. In instances in which the process involves the bulk of the lower extremity, amputation rather than attempts at revascularization may be the most prudent course to prevent the toxic product in the ischemic limb from entering the systemic circulation.
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23

Meadows, Kristy L. "Experimental models of focal and multifocal cerebral ischemia: a review." Reviews in the Neurosciences 29, no. 6 (August 28, 2018): 661–74. http://dx.doi.org/10.1515/revneuro-2017-0076.

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AbstractRodent and rabbit stroke models have been instrumental in our current understanding of stroke pathophysiology; however, translational failure is a significant problem in preclinical ischemic stroke research today. There are a number of different focal cerebral ischemia models that vary in their utility, pathophysiology of causing disease, and their response to treatments. Unfortunately, despite active preclinical research using these models, treatment options for ischemic stroke have not significantly advanced since the food and drug administration approval of tissue plasminogen activator in 1996. This review aims to summarize current stroke therapies, the preclinical experimental models used to help develop stroke therapies, as well as their advantages and limitations. In addition, this review discusses the potential for naturally occurring canine ischemic stroke models to compliment current preclinical models and to help bridge the translational gap between small mammal models and human clinical trials.
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24

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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25

Semenza, Gregg L. "Series Introduction: Tissue ischemia: pathophysiology and therapeutics." Journal of Clinical Investigation 106, no. 5 (September 1, 2000): 613–14. http://dx.doi.org/10.1172/jci10913.

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26

Goldstein, James A. "Pathophysiology and management of right heart ischemia." Journal of the American College of Cardiology 40, no. 5 (September 2002): 841–53. http://dx.doi.org/10.1016/s0735-1097(02)02048-x.

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27

Benjamin, Ernest, and John M. Oropello. "Acute mesenteric ischemia: Pathophysiology, diagnosis, and treatment." Disease-a-Month 39, no. 3 (March 1993): 134–210. http://dx.doi.org/10.1016/0011-5029(93)90023-v.

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28

Signorelli, Salvatore Santo, Luca Vanella, Nader G. Abraham, Salvatore Scuto, Elisa Marino, and Petra Rocic. "Pathophysiology of chronic peripheral ischemia: new perspectives." Therapeutic Advances in Chronic Disease 11 (January 2020): 204062231989446. http://dx.doi.org/10.1177/2040622319894466.

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Peripheral arterial disease (PAD) affects individuals particularly over 65 years old in the more advanced countries. Hemodynamic, inflammatory, and oxidative mechanisms interact in the pathophysiological scenario of this chronic arterial disease. We discuss the hemodynamic, muscle tissue, and oxidative stress (OxS) conditions related to chronic ischemia of the peripheral arteries. This review summarizes the results of evaluating both metabolic and oxidative markers, and also therapy to counteract OxS. In conclusion, we believe different pathways should be highlighted to discover new drugs to treat patients suffering from PAD.
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29

Bulkley, Gregory B., Atsushi Oshima, and Robert W. Bailey. "Pathophysiology of hepatic ischemia in cardiogenic shock." American Journal of Surgery 151, no. 1 (January 1986): 87–97. http://dx.doi.org/10.1016/0002-9610(86)90017-6.

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30

Morris, James J. "Silent Myocardial Ischemia: Pathophysiology and Clinical Recognition." Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy 7, no. 5P2 (September 10, 1987): S—56—S—61. http://dx.doi.org/10.1002/j.1875-9114.1987.tb04051.x.

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31

Silva, Cristiane Iozzi, Paulo Cézar Novais, Andressa Romualdo Rodrigues, Camila A. M. Carvalho, Benedicto Oscar Colli, Carlos Gilberto Carlotti Jr., Luís Fernando Tirapelli, and Daniela P. C. Tirapelli. "Expression of NMDA receptor and microRNA-219 in rats submitted to cerebral ischemia associated with alcoholism." Arquivos de Neuro-Psiquiatria 75, no. 1 (January 2017): 30–35. http://dx.doi.org/10.1590/0004-282x20160188.

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ABSTRACT Alcohol consumption aggravates injuries caused by ischemia. Many molecular mechanisms are involved in the pathophysiology of cerebral ischemia, including neurotransmitter expression, which is regulated by microRNAs. Objective: To evaluate the microRNA-219 and NMDA expression in brain tissue and blood of animals subjected to cerebral ischemia associated with alcoholism. Methods: Fifty Wistar rats were divided into groups: control, sham, ischemic, alcoholic, and ischemic plus alcoholic. The expression of microRNA-219 and NMDA were analyzed by real-time PCR. Results: When compared to the control group, the microRNA-219 in brain tissue was less expressed in the ischemic, alcoholic, and ischemic plus alcoholic groups. In the blood, this microRNA had lower expression in alcoholic and ischemic plus alcoholic groups. In the brain tissue the NMDA gene expression was greater in the ischemic, alcoholic, and ischemic plus alcoholic groups. Conclusion: A possible modulation of NMDA by microRNA-219 was observed with an inverse correlation between them.
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32

Sutton, Timothy A., Henry E. Mang, Silvia B. Campos, Ruben M. Sandoval, Mervin C. Yoder, and Bruce A. Molitoris. "Injury of the renal microvascular endothelium alters barrier function after ischemia." American Journal of Physiology-Renal Physiology 285, no. 2 (August 2003): F191—F198. http://dx.doi.org/10.1152/ajprenal.00042.2003.

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The role of renal microvascular endothelial cell injury in the pathophysiology of ischemic acute renal failure (ARF) remains largely unknown. No consistent morphological alterations have been ascribed to the endothelium of the renal microvasculature as a result of ischemia-reperfusion injury. Therefore, the purpose of this study was to examine biochemical markers of endothelial injury and morphological changes in the renal microvascular endothelium in a rodent model of ischemic ARF. Circulating von Willebrand factor (vWF) was measured as a marker of endothelial injury. Twenty-four hours after ischemia, circulating vWF peaked at 124% over baseline values ( P = 0.001). The FVB-TIE2/GFP mouse was utilized to localize morphological changes in the renal microvascular endothelium. Immediately after ischemia, there was a marked increase in F-actin aggregates in the basal and basolateral aspect of renal microvascular endothelial cells in the corticomedullary junction. After 24 h of reperfusion, the pattern of F-actin staining was more similar to that observed under physiological conditions. In addition, alterations in the integrity of the adherens junctions of the renal microvasculature, as demonstrated by loss of localization in vascular endothelial cadherin immunostaining, were observed after 24 h of reperfusion. This observation temporally correlated with the greatest extent of permeability defect in the renal microvasculature as identified using fluorescent dextrans and two-photon intravital imaging. Taken together, these findings indicate that renal vascular endothelial injury occurs in ischemic ARF and may play an important role in the pathophysiology of ischemic ARF.
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33

Moyon, Anaïs, Philippe Garrigue, Laure Balasse, Samantha Fernandez, Pauline Brige, Ahlem Bouhlel, Guillaume Hache, Françoise Dignat-George, David Taïeb, and Benjamin Guillet. "Succinate Injection Rescues Vasculature and Improves Functional Recovery Following Acute Peripheral Ischemia in Rodents: A Multimodal Imaging Study." Cells 10, no. 4 (April 2, 2021): 795. http://dx.doi.org/10.3390/cells10040795.

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Succinate influences angiogenesis and neovascularization via a hormonelike effect on G-protein-coupled receptor 91 (GPR91). This effect has been demonstrated in the pathophysiology of diabetic retinopathy and rheumatoid arthritis. To evaluate whether succinate can play a role in acute peripheral ischemia, a preclinical study was conducted with ischemic mice treated with succinate or PBS and evaluated by imaging. Acute ischemia was followed by an increased in GPR91 expression in the ischemic muscle. As assessed with LASER-Doppler, succinate treatment resulted in an earlier and more intense reperfusion of the ischemic hindlimb compared to the control group (* p = 0.0189). A microPET study using a radiolabeled integrin ligand ([68Ga]Ga-RGD2) showed an earlier angiogenic activation in the succinate arm compared to control mice (* p = 0.020) with a prolonged effect. Additionally, clinical recovery following ischemia was better in the succinate group. In conclusion, succinate injection promotes earlier angiogenesis after ischemia, resulting in a more effective revascularization and subsequently a better functional recovery.
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34

Azad, Tej D., Anand Veeravagu, and Gary K. Steinberg. "Neurorestoration after stroke." Neurosurgical Focus 40, no. 5 (May 2016): E2. http://dx.doi.org/10.3171/2016.2.focus15637.

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Recent advancements in stem cell biology and neuromodulation have ushered in a battery of new neurorestorative therapies for ischemic stroke. While the understanding of stroke pathophysiology has matured, the ability to restore patients' quality of life remains inadequate. New therapeutic approaches, including cell transplantation and neurostimulation, focus on reestablishing the circuits disrupted by ischemia through multidimensional mechanisms to improve neuroplasticity and remodeling. The authors provide a broad overview of stroke pathophysiology and existing therapies to highlight the scientific and clinical implications of neurorestorative therapies for stroke.
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35

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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36

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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37

Goldstein, James A. "Pathophysiology and clinical management of right heart ischemia." Current Opinion in Cardiology 14, no. 4 (July 1999): 329–39. http://dx.doi.org/10.1097/00001573-199907000-00009.

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38

Gaehtgens, P., and P. Marx. "Hemorheological Aspects of the Pathophysiology of Cerebral Ischemia." Journal of Cerebral Blood Flow & Metabolism 7, no. 3 (June 1987): 259–65. http://dx.doi.org/10.1038/jcbfm.1987.61.

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39

Maiese, Kenneth. "Cerebral Ischemia: Molecular and Cellular Pathophysiology. Wolfgang Walz." Quarterly Review of Biology 75, no. 3 (September 2000): 364–65. http://dx.doi.org/10.1086/393612.

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40

Smith, Wade S. "Pathophysiology of Focal Cerebral Ischemia: a Therapeutic Perspective." Journal of Vascular and Interventional Radiology 15, no. 1 (January 2004): S3—S12. http://dx.doi.org/10.1097/01.rvi.0000108687.75691.0c.

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41

Mifsud, Gabriella, Christian Zammit, Richard Muscat, Giuseppe Di Giovanni, and Mario Valentino. "Oligodendrocyte Pathophysiology and Treatment Strategies in Cerebral Ischemia." CNS Neuroscience & Therapeutics 20, no. 7 (April 7, 2014): 603–12. http://dx.doi.org/10.1111/cns.12263.

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42

Vetrovec, George W. "Changing concepts in the pathophysiology of myocardial ischemia." American Journal of Cardiology 64, no. 11 (September 1989): F3—F9. http://dx.doi.org/10.1016/0002-9149(89)90739-x.

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43

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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44

Ma, Qingyi, Lubo Zhang, and William J. Pearce. "MicroRNAs in brain development and cerebrovascular pathophysiology." American Journal of Physiology-Cell Physiology 317, no. 1 (July 1, 2019): C3—C19. http://dx.doi.org/10.1152/ajpcell.00022.2019.

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MicroRNAs (miRNAs) are a class of highly conserved non-coding RNAs with 21–25 nucleotides in length and play an important role in regulating gene expression at the posttranscriptional level via base-paring with complementary sequences of the 3′-untranslated region of the target gene mRNA, leading to either transcript degradation or translation inhibition. Brain-enriched miRNAs act as versatile regulators of brain development and function, including neural lineage and subtype determination, neurogenesis, synapse formation and plasticity, neural stem cell proliferation and differentiation, and responses to insults. Herein, we summarize the current knowledge regarding the role of miRNAs in brain development and cerebrovascular pathophysiology. We review recent progress of the miRNA-based mechanisms in neuronal and cerebrovascular development as well as their role in hypoxic-ischemic brain injury. These findings hold great promise, not just for deeper understanding of basic brain biology but also for building new therapeutic strategies for prevention and treatment of pathologies such as cerebral ischemia.
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45

Calise, Justine, and Saul R. Powell. "The ubiquitin proteasome system and myocardial ischemia." American Journal of Physiology-Heart and Circulatory Physiology 304, no. 3 (February 1, 2013): H337—H349. http://dx.doi.org/10.1152/ajpheart.00604.2012.

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The ubiquitin proteasome system (UPS) has been the subject of intensive research over the past 20 years to define its role in normal physiology and in pathophysiology. Many of these studies have focused in on the cardiovascular system and have determined that the UPS becomes dysfunctional in several pathologies such as familial and idiopathic cardiomyopathies, atherosclerosis, and myocardial ischemia. This review presents a synopsis of the literature as it relates to the role of the UPS in myocardial ischemia. Studies have shown that the UPS is dysfunctional during myocardial ischemia, and recent studies have shed some light on possible mechanisms. Other studies have defined a role for the UPS in ischemic preconditioning which is best associated with myocardial ischemia and is thus presented here. Very recent studies have started to define roles for specific proteasome subunits and components of the ubiquitination machinery in various aspects of myocardial ischemia. Lastly, despite the evidence linking myocardial ischemia and proteasome dysfunction, there are continuing suggestions that proteasome inhibitors may be useful to mitigate ischemic injury. This review presents the rationale behind this and discusses both supportive and nonsupportive studies and presents possible future directions that may help in clarifying this controversy.
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46

Liu, Shimin, Honglian Shi, Wenlan Liu, Takamitsu Furuichi, Graham S. Timmins, and Ke Jian Liu. "Interstitial pO2 in Ischemic Penumbra and Core are Differentially Affected following Transient Focal Cerebral Ischemia in Rats." Journal of Cerebral Blood Flow & Metabolism 24, no. 3 (March 2004): 343–49. http://dx.doi.org/10.1097/01.wcb.0000110047.43905.01.

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Stroke causes heterogeneous changes in tissue oxygenation, with a region of decreased blood flow, the penumbra, surrounding a severely damaged ischemic core. Treatment of acute ischemic stroke aims to save this penumbra before its irreversible damage by continued ischemia. However, effective treatment remains elusive due to incomplete understanding of processes leading to penumbral death. While oxygenation is central in ischemic neuronal death, it is unclear exactly what actual changes occur in interstitial oxygen tension (pO2) in ischemic regions during stroke, particularly the penumbra. Using the unique capability of in vivo electron paramagnetic resonance (EPR) oximetry to measure localized interstitial pO2, we measured both absolute values, and temporal changes of pO2 in ischemic penumbra and core during ischemia and reperfusion in a rat model. Ischemia rapidly decreased interstitial pO2 to 32% ± 7.6% and 4% ± 0.6% of pre-ischemic values in penumbra and core, respectively 1 hour after ischemia. Importantly, whilst reperfusion restored core pO2 close to its pre-ischemic value, penumbral pO2 only partially recovered. Hyperoxic treatment significantly increased penumbral pO2 during ischemia, but not in the core, and also increased penumbral pO2 during reperfusion. These divergent, important changes in pO2 in penumbra and core were explained by combined differences in cellular oxygen consumption rates and microcirculation conditions. We therefore demonstrate that interstitial pO2 in penumbra and core is differentially affected during ischemia and reperfusion, providing new insights to the pathophysiology of stroke. The results support normobaric hyperoxia as a potential early intervention to save penumbral tissue in acute ischemic stroke.
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47

Baird, Alison E., and Steven Warach. "Magnetic Resonance Imaging of Acute Stroke." Journal of Cerebral Blood Flow & Metabolism 18, no. 6 (June 1998): 583–609. http://dx.doi.org/10.1097/00004647-199806000-00001.

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In the investigation of ischemic stroke, conventional structural magnetic resonance (MR) techniques (e.g., T1-weighted imaging, T2-weighted imaging, and proton density-weighted imaging) are valuable for the assessment of infarct extent and location beyond the first 12 to 24 hours after onset, and can be combined with MR angiography to noninvasively assess the intracranial and extracranial vasculature. However, during the critical first 6 to 12 hours, the probable period of greatest therapeutic opportunity, these methods do not adequately assess the extent and severity of ischemia. Recent developments in functional MR imaging are showing great promise for the detection of developing focal cerebral ischemic lesions within the first hours. These include (1) diffusion-weighted imaging, which provides physiologic information about the self-diffusion of water, thereby detecting one of the first elements in the pathophysiologic cascade leading to ischemic injury; and (2) perfusion imaging. The detection of acute intraparenchymal hemorrhagic stroke by susceptibility weighted MR has also been reported. In combination with MR angiography, these methods may allow the detection of the site, extent, mechanism, and tissue viability of acute stroke lesions in one imaging study. Imaging of cerebral metabolites with MR spectroscopy along with diffusion-weighted imaging and perfusion imaging may also provide new insights into ischemic stroke pathophysiology. In light of these advances in structural and functional MR, their potential uses in the study of the cerebral ischemic pathophysiology and in clinical practice are described, along with their advantages and limitations.
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48

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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49

Sabri, Mohammed, Elliot Lass, and R. Loch Macdonald. "Early Brain Injury: A Common Mechanism in Subarachnoid Hemorrhage and Global Cerebral Ischemia." Stroke Research and Treatment 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/394036.

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Early brain injury (EBI) has become an area of extreme interest in the recent years and seems to be a common denominator in the pathophysiology of global transient ischemia and subarachnoid hemorrhage (SAH). In this paper, we highlight the importance of cerebral hypoperfusion and other mechanisms that occur in tandem in both pathologies and underline their possible roles in triggering brain injury after hemorrhagic or ischemic strokes.
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50

Patel, Hemanshu, Cissy Yong, Ali Navi, Sidney G. Shaw, Xu Shiwen, David Abraham, Daryll M. Baker, and Janice CS Tsui. "Toll-like receptors 2 and 6 mediate apoptosis and inflammation in ischemic skeletal myotubes." Vascular Medicine 24, no. 4 (May 14, 2019): 295–305. http://dx.doi.org/10.1177/1358863x19843180.

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Critical limb ischemia (CLI) is associated with skeletal muscle damage. However, the pathophysiology of the muscle damage is poorly understood. Toll-like receptors (TLR) have been attributed to play a role in ischemia-induced tissue damage but their role in skeletal muscle damage in CLI is unknown. TLR2 and TLR6 expression was found to be upregulated in skeletal muscle of patients with CLI. In vitro, ischemia led to upregulation of TLR2 and TLR6 by myotubes, and activation of the downstream TLR signaling pathway. Ischemia-induced activation of the TLR signaling pathway led to secretion of the pro-inflammatory cytokine interleukin-6 and muscle apoptosis, which were abrogated by neutralising TLR2 and TLR6 antibodies. Our study demonstrates that TLR2 and TLR6 are upregulated in ischemic muscle and play a role in ischemia-induced muscle damage. Thus, manipulating the TLR pathway locally may be of potential therapeutic benefit.
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