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Academic literature on the topic 'Ischemia – Pathophysiology'

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Published: 4 June 2021
Last updated: 21 February 2023

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Journal articles on the topic "Ischemia – Pathophysiology"

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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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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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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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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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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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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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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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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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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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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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Dissertations / Theses on the topic "Ischemia – Pathophysiology"

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Christensen, Thomas. "Experimental focal cerebral ischemia : pathophysiology, metabolism and pharmacology of the ischemic penumbra /." Copenhagen, 2007. http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&doc_number=016143698&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA.

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Li, Ping-An. "Mechanisms of acidosis-mediated ischemic brain damage histopathology and pathophysiology /." Lund : Lund University, 1996. http://catalog.hathitrust.org/api/volumes/oclc/38158955.html.

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White, Melanie Yvonne. "Proteomics of ischemia/reperfusion injury in rabbit myocardium." Thesis, The University of Sydney, 2006. https://hdl.handle.net/2123/27890.

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Myocardial stunning is best defined as the persistent, yet reversible, contractile dysfunction that occurs with brief myocardial ischemia / reperfusion (I/R) injury. In contrast, prolonged ischemia results in myocardial infarction that leads to cell death of necrosis of the tissue. The causes of stunning are not fully elucidated, however two major hypotheses currently exist; firstly changes to calcium handling resulting from lowered cellular pH by means of anaerobic respiration, and altered Nair/H)r antiporter kinetics, and secondly, the generation oxygen free radical (OFR) that may occur in a dramatic ‘surge’ at the onset of reperfusion. Treatment of ischemic myocardium with calcium channel blockers and / or OFR scavengers has been successfully shown to prevent stunning in various animal models. Whilst much is known about the physiological and biochemical changes that occur in stunned myocardium, very little is known about events at the molecular level. Since stunning occurs after only brief (15 minutes low-flow in the rabbit model) ischemia and subsequent reperfusion, we hypothesized that these molecular events are not predominated by large changes in protein expression and abundance, yet rather by subtle and / or transient changes to protein post-translational modifications (PTM). Such changes at the protein level are best analysed using the technologies encompassed under the term ‘proteomics’.
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Sevastos, Jacob Prince of Wales Clinical School UNSW. "The role of tissue factor in renal ischaemia reperfusion injury." Awarded by:University of New South Wales. Prince of Wales Clinical School, 2006. http://handle.unsw.edu.au/1959.4/27416.

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Reperfusion injury may mediate renal dysfunction following ischaemia. A murine model was developed to investigate the role of the tissue factor-thrombin-protease activated receptor pathway in renal ischaemia reperfusion injury (IRI). In this model, mice received 25 minutes of ischaemia and subsequent periods of reperfusion. C57BL6, protease activated receptor-1 (PAR-1) knockout mice, and tissue factor (TF) deficient mice were used. Following 24 hours IRI, PAR-1 deficiency resulted in protection against severe renal failure compared to the C57BL6 mice (creatinine, 118.2 ?? 6.3 vs 203 ?? 12 ??mol/l, p<0.001). This was confirmed by lesser tubular injury. By 48 hours IRI, this resulted in a survival benefit (survival, 87.5% vs 0%, p<0.001). Treatment of C57BL6 mice with hirudin, a specific thrombin inhibitor, offered renoprotection at 24 hours IRI (creatinine, 107 ?? 10 ??mol/l, p<0.001), leading to a 60% survival rate at 48 hours IRI (p<0.001). TF deficient mice expressing less than 1% of C57BL6 mouse TF were also protected (creatinine, 113.6 ?? 7 ??mol/l, p<0.001), with a survival benefit of 75% (p<0.001). The PAR-1 knockout, hirudin treated C57BL6 and TF deficient mice had reduced myeloperoxidase activity and tissue neutrophil counts compared to the C57BL6 mice, along with reduced KC and MIP-2 chemokine mRNA and protein expression. Hirudin treatment of PAR-1 knockout mice had no additional benefit over PAR-1 absence alone, suggesting no further contribution by activation of other protease activated receptors (creatinine at 24 hours IRI, 106.5 ?? 10.5 ??mol/l, p>0.05). Furthermore, immunofluoresence staining for fibrin(ogen) showed no difference between C57BL6 and PAR-1 knockout mice, suggesting no major contribution by fibrin in this model. Renal IRI resulted in increased levels of TF mRNA expression in the C57BL6, PAR-1 knockout, and hirudin treated C57BL6 mice compared to normal controls, suggesting that TF mRNA expression was upregulated in this model. This resulted in increased TF functional activity in the C57BL6 and PAR-1 knockout mice, but TF activity was negligible in hirudin treated C57BL6 and TF deficient mice. The data therefore suggests that the TF-thrombin cascade contributes to renal IRI by signalling via PAR-1 that then regulates chemokine gene expression and subsequent neutrophil recruitment.
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Nechytailo, O. Yu. "Pathophysiology of the lower limbs critical ischemia in patients with type 2 diabetes mellitus." Thesis, БДМУ, 2021. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/19107.

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Nicolaou, Persoulla. "The Role of Inhibitor-1 and Heat Shock Protein 20 in Cardiac Pathophysiology." University of Cincinnati / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1227108454.

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Halldner, Henriksson Linda. "Physiology and pathophysiology of central adenosine A1 and A2A receptors /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-628-5732-0/.

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Pucheu, Sylvie. "Contribution à l'étude des manifestations physiopathologiques liées au stress oxydatif intervenant lors de la reperfusion du myocarde ischémique : rôle des oligoéléments et essais de protection par des molécules antioxydantes." Université Joseph Fourier (Grenoble ; 1971-2015), 1994. http://www.theses.fr/1994GRE10180.

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Le present travail s'inscrit dans le cadre general des etudes consacrees a la protection pharmacologique du tissu cardiaque reperfuse apres une periode d'ischemie de courte duree. Les differentes etudes experimentales qui le constituent sont realisees sur un modele d'ischemie myocardique sur le cur isole et perfuse de rat, et prennent en compte une appreciation fonctionnelle, ultrastructurale et metabolique des effets du cycle ischemie-reperfusion. Une etude clinique, s'inscrivant dans une thematique voisine, complete l'ensemble. Dans la premiere partie de ce travail, nous avons mis en evidence l'implication des radicaux libres de l'oxygene, via la reaction de fenton, dans le developpement des lesions d'ischemie-reperfusion. Nous avons montre qu'une surcharge myocardique en fer augmentait la susceptibilite du tissu cardiaque vis a vis d'un cycle d'ischemie-reperfusion. En revanche, nous avons observe un effet benefique de la surcharge en fer sur l'incidence des troubles du rythme a la reperfusion. Enfin, nous avons montre qu'un traitement par des antioxydants et plus particulierement par l'euk8, molecule presentant in vitro une forte activite de type sod et catalase, entrainait une importante diminution des alterations fonctionnelles et ultrastructurales des curs surcharges en fer a la reperfusion. Dans la seconde partie, nous avons etudie le role des oligoelements (zn, cu, se et mn), cofacteurs d'enzymes de defense antiradicalaire, dans le developpement des lesions cellulaires associees a la reperfusion post-ischemique. Nous avons d'une part mis en evidence une plus grande vulnerabilite du tissu cardiaque dans les monocarences en oligoelements et plus particulierement dans les carences en selenium ou en cuivre. D'autre part, nous avons montre qu'un apport nutritionnel simultane en ces divers oligoelements augmentait l'activite des enzymes antioxydantes, limitant ainsi les consequences fonctionnelles et structurales de l'ischemie et de la reperfusion. Enfin, une troisieme partie consacree a l'etude de l'existence d'un stress radicalaire chez des patients presentant un infarctus du myocarde traite par thrombolyse, a permis de montrer 1) que les dosages plasmatiques des mda et de la gpx constituent un bon reflet de la production radicalaire apres traitement thrombolytique, et 2) que les systemes antioxydants physiologiques apparaissent modifies chez ces patients
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Roach, Denise Margaret. "Upregulation of matrix metalloproteinases -2 and -9 and type IV collagen degradation in skeletal muscle reperfusion injury." Title page, contents and abstract only, 2002. http://web4.library.adelaide.edu.au/theses/09MD/09mdr6281.pdf.

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Includes bibliographical references (leaves 292-352) Determines the role of matrix metalloproteinases, MMP-2 and MMP-9 in reperfusion injury following skeletal muscle ischaemia; and, whether inhibition of MMPs by doxycycline protects against tissue damage.
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Fernández, Sanz Celia. "Defective sarcoplasmic reticulum-mitochondria communication in aged heart and its effect on ischemia and reperfusion injury." Doctoral thesis, Universitat Autònoma de Barcelona, 2015. http://hdl.handle.net/10803/323906.

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Las alteraciones mitocondriales están vinculadas a la mayor vulnerabilidad de padecer enfermedades durante el envejecimiento. La edad avanzada es un factor determinante de la incidencia y gravedad de la cardiopatía isquémica. Estudios preclínicos sugieren la existencia de un daño celular intrínseco, por mecanismos no del todo establecidos, que contribuye a un incremento de la susceptibilidad del miocardio senescente al daño isquémico. Esta tesis investiga el papel de la comunicación mitocondria-retículo sarcoplásmico (RS) en el deterioro funcional de los cardiomiocitos durante el envejecimiento. El estudio ecocardiográfico ha demostrado que la función cardiaca en el reposo se mantiene preservada en los animales viejos. No se han observado cambios debidos a la edad en el potencial de membrana mitocondrial ni en el consumo de oxígeno en condiciones de reposo en mitocondrias aisladas de corazones de ratón. El consumo de oxígeno inducido por ADP ha revelado que las mitocondrias interfibrilares de corazones viejos no alcanzan el nivel respiratorio máximo. Análisis proteómicos de segunda generación han demostrado un aumento de la oxidación de proteínas mitocondriales relacionado con el envejecimiento. Esta tesis ha investigado el posible efecto de la edad sobre la capacidad de las mitocondrias para captar calcio. En cardiomiocitos la captación mitocondrial del calcio procedente del RS se ha visto reducida de forma significativa en el envejecimiento. Esta disminución de la captación de calcio mitocondrial se asoció a una reducida capacidad de regeneración de NAD(P)H y a un incremento de la producción de ROS mitocondriales en cardiomiocitos viejos. Ensayos de inmunofluorescencia y de ligación por proximidad han revelado una comunicación defectuosa entre la mitocondria y el RS en cardiomiocitos de corazones senescentes. La desestructuración de las uniones entre el RS y la mitocondria con colchicina fue capaz de reproducir el efecto de la edad sobre las alteraciones en el manejo/transferencia de calcio entre ambos orgánulos en cardiomiocitos jóvenes. La segunda parte de este trabajo investiga el impacto potencial de las alteraciones mitocondriales sobre los efectos adversos del envejecimiento en el daño por isquemia y reperfusión (IR). Los corazones aislados y perfundidos de ratones viejos sometidos a IR desarrollaron mayor rotura sarcolemal y tamaño de infarto, junto con un retraso significativo del desarrollo del rigor isquémico. Los cardiomiocitos viejos sometidos a isquemia, desarrollaron una caída más rápida del potencial de membrana mitocondrial (ΔΨm) junto con un retraso paradójico en la aparición del rigor. La tasa de recuperación transitoria del ΔΨm durante los primeros minutos de isquemia, debida a la actividad reversa de la FoF1-ATPsintasa, se encontró significativamente disminuida en cardiomiocitos viejos. El análisis proteómico ha demostrado un aumento de la oxidación de diferentes subunidades de la FoF1-ATPsintasa asociado al envejecimiento. La alteración del ΔΨm observado en los cardiomiocitos viejos se asoció a una menor captación de calcio mitocondrial durante la IR. A pesar de esto, el desarrollo de permeabilidad transitoria (mPT) fue mayor en los cardiomiocitos senescentes y este efecto se correlacionó con una mayor hipercontractura y muerte celular en reperfusión. Por lo tanto, el desarrollo de una comunicación defectuosa entre el RS y la mitocondria durante el envejecimiento produce un intercambio ineficiente de calcio entre ambos orgánulos, que contribuye al desajuste en la demanda/aporte de energía y a un aumento consiguiente del estrés oxidativo. La oxidación de la FoF1-ATPsintasa se asocia a una alteración de su funcionamiento y a un incremento de la sensibilidad de la mitocondria para desarrollar mPT. Debido al modelo recientemente propuesto según el cual la FoF1-ATPsintasa forma parte del mPTP, es posible especular que la oxidación de esta enzima está asociada al aumento del daño por IR en el miocardio senescente.
Mitochondrial alterations are critically involved in the increased vulnerability to disease during aging. On the other hand, aging is a major determinant of the incidence and severity of ischemic heart disease. Preclinical information suggests the existence of intrinsic cellular alterations that contribute to ischemic susceptibility in senescent myocardium, by mechanisms not well established. The first part of this thesis investigates the contribution of mitochondria-sarcoplasmic reticulum (SR) communication in the functional decline of cardiomyocyte during aging. Echochardiographic analysis of aging mice (>20 months) showed a rather preserved cardiac contractile function in resting conditions respect to young mice (5-6 months). ATP/phosphocreatine were preserved in hearts from old mice as quantified by RMN spectroscopy. In isolated mitochondria from young and old mouse hearts, mitochondrial membrane potential and resting O2 consumption were similar in both groups. However, stimulation of O2 consumption after the addition of ADP resulted in a partial failure of interfibrillar mitochondria from aged hearts to achieve maximal respiratory rate. Second generation proteomics disclosed an increase of mitochondrial protein oxidation in advanced age. Because both energy production and oxidative status are regulated by mitochondrial calcium, this work further investigated the effect of age on mitochondrial calcium uptake. While no age-dependent differences were found in calcium uptake kinetics in isolated mitochondria, in which the contribution of other organelles and sarcolemma is absent, mitochondrial calcium uptake secondary to SR calcium release was significantly reduced in cardiomyocytes from old hearts. Reduced mitochondrial calcium uptake in aging cardiomyocytes was associated with decreased NAD(P)H regeneration and a concomitant increase of mitochondrial ROS production manifested only when cells were exposed to high frequency electrical stimulation. Immunofluorescence and proximity ligation assay identified defective communication between mitochondria and SR in cardiomyocytes from aged hearts. Functional analysis of calcium handling in fluo-4 loaded cardiomyocytes disclosed an altered pattern of RyR gating properties. The observed defects in SR calcium transfer and in calcium handling could be reproduced in young cardiomyocytes after interorganelle disruption with colchicine, at concentrations that had no significant effect in aged cardiomyocytes or isolated mitochondria. The second part of this work investigates the potential impact of the altered mitochondrial function in the adverse effect of aging on myocardial ischemia and reperfusion (IR) injury. Isolated perfused hearts from old mice submitted to transient IR displayed an increase in hypercontracture, sarcolemmal rupture and infarct size, as compared to hearts from young mice, despite a paradoxical delay ischemic rigor contracture onset. In isolated cardiomyocytes from aging hearts submitted to IR there was a faster decline of mitochondrial membrane potential (ΔΨm) in comparison with young ones, but ischemic rigor shortening was also delayed. Transient recovery of ΔΨm observed during ischemia, secondary to the reversal of mitochondrial FoF1-ATPsynthase to ATPase mode, was markedly reduced in aging cardiomyocytes. Proteomic analysis demonstrated an increased oxidation of different subunits of FoF1-ATPsynthase. Altered bionergetics in aging cells was associated with reduced mitochondrial calcium uptake and more severe cytosolic calcium overload during both ischemia and reperfusion. Despite attenuated mitochondrial calcium overload, the occurrence of mitochondrial permeability transition pore (mPTP) opening, hypercontracture and cell death were increased during reperfusion in cardiomyocytes from old mice. In vitro studies demonstrated a significantly reduced calcium retention capacity in interfibrillar mitochondria from aging hearts. Thus, defective SR-mitochondria communication underlies inefficient interorganelle calcium exchange that contributes to energy demand/supply mismatch and oxidative stress in the aged heart. This may spread on an altered FoF1-ATPsynthase and increased sensitivity of mitochondria to undergo mPTP opening as important determinants of the reduced tolerance to ischemia-reperfusion in senescent myocardium. Because ATPsynthase has been proposed to conform mPTP, it is tempting to hypothesize that oxidation of ATPsynthase underlie both phenomena.
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Books on the topic "Ischemia – Pathophysiology"

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A, Schurr, and Rigor Benjamin M, eds. Cerebral ischemia and resuscitation. Boca Raton: CRC Press, 1990.

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Gusev, E. I. Brain ischemia. New York: Kluwer Academic/Plenum Publishers, 2003.

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Heusch, Gerd, ed. Pathophysiology and Rational Pharmacotherapy of Myocardial Ischemia. Heidelberg: Steinkopff, 1990. http://dx.doi.org/10.1007/978-3-642-54133-9.

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1944-, Cohen Michael V., ed. Myocardial ischemia and reperfusion. Dordrecht: Kluwer Academic Publishers, 1998.

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1946-, Das Dipak Kumar, ed. Pathophysiology of reperfusion injury. Boca Raton: CRC Press, 1993.

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Marston, Adrian. Vascular disease of the gut: Pathophysiology, recognition and management. 2nd ed. London: Edward Arnold, 1986.

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1932-, Abiko Yasushi, and Karmazyn M. 1950-, eds. Protection against ischemia/reperfusion damage of the heart. Tokyo: Springer, 1998.

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V, Cokkinos Dennis, ed. Myocardial ischemia: From mechanisms to therapeutic potentials. New York: Springer, 2005.

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Ostadal, Bohuslav. Cardiac ischemia: From injury to protection. Boston: Kluwer Academic Publishers, 1999.

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František, Kolář, ed. Cardiac ischemia: From injury to protection. Boston: Kluwer Academic Publishers, 1999.

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Book chapters on the topic "Ischemia – Pathophysiology"

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Hacke, Werner, Herman J. Gelmers, Michael Hennerici, and Günter Krämer. "Pathophysiology of Cerebral Ischemia." In Cerebral Ischemia, 17–30. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-75548-4_2.

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Malliani, A. "Pathophysiology of ischemic cardiac pain." In Silent Ischemia, 19–24. Heidelberg: Steinkopff, 1987. http://dx.doi.org/10.1007/978-3-662-12997-5_3.

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Ropper, A. H. "Pathophysiology of Raised Intracranial Pressure." In Brain Ischemia, 269–72. London: Springer London, 1995. http://dx.doi.org/10.1007/978-1-4471-2073-5_27.

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Özben, Tomris. "Pathophysiology of Cerebral Ischemia." In Free Radicals, Oxidative Stress, and Antioxidants, 163–87. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4757-2907-8_17.

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Rozanski, Alan, and D. Berman. "The frequency, pathophysiology, and prognosis of exercise-induced silent ischemia." In Silent Ischemia, 96–106. Heidelberg: Steinkopff, 1987. http://dx.doi.org/10.1007/978-3-662-12997-5_13.

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Sloan, M. A. "Cerebral Vasoconstriction: Physiology, Pathophysiology and Occurrence in Selected Cerebrovascular Disorders." In Brain Ischemia, 151–72. London: Springer London, 1995. http://dx.doi.org/10.1007/978-1-4471-2073-5_18.

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Mangano, Dennis T. "Myocardial Ischemia: Pathophysiology and Detection." In Anesthesiology 1986, 36–49. Dordrecht: Springer Netherlands, 1986. http://dx.doi.org/10.1007/978-94-009-4251-6_6.

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Hurn, P. D., A. Bhardwaj, and R. J. Traystman. "Cerebral Ischemia: Pathophysiology and Neuroprotection." In Mechanisms of Organ Dysfunction in Critical Illness, 339–47. Berlin, Heidelberg: Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-642-56107-8_24.

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Pepine, Carl. "Pathophysiology of Ischemia: Why are Some Episodes Silent?" In Silent Myocardial Ischemia, 7–15. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-1745-6_2.

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Lazzara, Ralph, and Benjamin J. Scherlag. "Cellular Electrophysiology and Ischemia." In Physiology and Pathophysiology of the Heart, 493–508. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0873-7_23.

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Conference papers on the topic "Ischemia – Pathophysiology"

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Araújo, Victor Oliveira, Isadora Mônica Ponte de Oliveira, Lara Maria de Oliveira Paiva Freitas, and Júlio César Claudino dos Santos. "“Brain fog” in the post-acute phase of Covid-19." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.681.

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Introduction: Covid-19 infection can affect not only the airways but also other organs such as the brain. Individuals that tested positive for SARSCoV-2 may be asymptomatic, but can also have symptoms - such as “brain fog” - during the acute phase and/or the post-acute phase (being the last ones defined as long haulers). “Brain fog” is a set of symptoms characterized by cognitive dysfunction that includes the inability to concentrate, executive function deficits, anterograde and retrograde amnesia. Objective: Review the pathophysiology of individuals with Covid-19 post-acute phase brain fog. Design and setting: A literature review was conducted on the topic. Methods: 12 original selected articles in English and Portuguese from PubMed and Google Academic databases dated from 2017 to 2021. Results: Research evidenced that 18-36% of the patients hospitalized for Covid-19 that had neurological symptoms also experienced brain fog in the post-acute phase. Although not completely elucidated, there are hypothesized mechanisms to clarify the neurological symptoms in the “long haulers’’ patients, such as the release of pro-inflammatory substances that reduce synaptic fidelity due to dysregulation in the levels of neurotransmitters which are fundamental for brain function. In addition, SARS-CoV-2 provides microthrombus formation and possible small cerebral ischemia. Conclusion: The pathophysiology of brain fog is not yet fully proven, since the literature on the subject is limited. Therefore, more robust research in patients who developed neurological symptoms after infection by the new coronavirus is needed to clarify the pathophysiology, clinical management and most appropriate treatment for individuals with brain fog.
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Martins, Karine Felipe, Flávia Pascoal Teles, Amanda Fernandes de Sousa Oliveira Balestra, and Isadora Rosa Maia. "Cerebrovascular diseases: the importance of recognizing them." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.188.

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Background: Until the 70s, cerebrovascular diseases (CVDs) were neglected to the lack of resources. However, due to the advancement of technology, several imaging tests have appeared, such as magnetic resonance and computed tomography, which facilitated the diagnosis and the understanding of the pathophysiology of each disease. Objectives: The objective of this work is to identify the main CVDs signs and symptoms. Methods: An integrative literature review was carried out based on selected articles from Google Scholar, PubMed and SciELO, using the terms headache, cerebrovascular disease, neurology. Results: CVDs are characterized by causing damage to brain vessels, due to changes in blood flow momentarily or permanently in an area of the brain, allowing them to be classified as ischemic or hemorrhagic. In ischemic there is a blockage of blood flow and, consequently, of oxygen to areas of the brain, in hemorrhagic rupture of a vessel occurs and, with this, blood leakage. Therefore, it is necessary to recognize the signs and symptoms early, in order to prevent loss of neurological function, movements on one side of the body and the presence or absence of headaches in both patients, with ischemic CVD and hemorrhagic CVD prevent rapid loss of consciousness accompanied by severe headache. Such signs and symptoms associated with the patient’s family history and lifestyle can help in the diagnosis of this disease. Conclusion: Therefore, it is important to recognize the signs and symptoms of CVDs, in order to determine the treatment and advise the patient, which will guarantee a better prognosis.
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Gastaldello, Gabriel Henrique, Amanda Rodrigues Correia Frota Gomes, Bruna Belone Garcia, Damiana Gianotto Pires, and Cristiane Tefé Sillva. "Pathogenesis and clinical aspects involved in stroke associated with COVID-19: A literature review." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.611.

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Introduction: Currently, an increasing number of studies point to the prevalence of neurological manifestations associated with COVID-19, including stroke. Although the pathophysiology is not completely understood, the infection induces a prothrombotic state stimulate by high levels of factor VIII, fibrinogen and Ddimer. In this sense, high mortality (44,2%) is a challenging context and identify influences of clinical and morphological aspects the outcome of these patients. Design and setting: Literature review conduced in Barão de Mauá University Center, Ribeirão Preto-SP. Objective: Clarifying aspects involved in the pathogenesis and clinical manifestations in patients with COVID-19 and Stroke. Methods: The primary databases utilized to retrieve the salient medical literature presented in this review were Scielo and Pubmed. The search terms, included “stroke”, “SARS-CoV”, “covid-19”. Discussion: Ischemic stroke was the most common subtype found associated with multiple infarctions and cryptogenic etiology. The mechanisms are multifactorial, including conventional pathways stimulated by the pathogen or direct action. Called “sepsis coagulopathy”, activation of the coagulation pathway associated with viral invasion of endothelial cells and excessive release of cytokines causes a prothrombotic state. Hemorrhagic stroke is less common. It is believed that the affinity of SARS-coV- 2 for ACE2 (angiotensinconverting enzyme 2) receptors could directly damage intracranial arteries, causing rupture, associated with fibrinogen depletion and massive release of cytokines and proteases. Conclusion: Individuals affected by COVID-19 that are affected by stroke face more severe conditions and worse associated outcomes. Thus, understanding the pathophysiology and clinical aspects brings greater effectiveness in the care of these individuals and lower mortality.
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Kindel, G., J. Fareed, and U. Cornelli. "EFFECTS OF DEFIBROTIDE TREATMENT ON THE PLASMA AND SERUM INDUCED CONTRACTION OF RABBIT AORTIC STRIP IN RELATION TO THE PATHOPHYSIOLOGY OF MYOCARDIAL INFARCTION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643147.

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Several clinical and experimental studies have demonstrated the efficacy of a polydeoxyribonucleotide (Defibrotide) in myocardial ischemic disorders and peripheral arterial diseases. In attempts to investigate the mechanisms of action of this agent, we used a modified rabbit model of hemodynamics and an isolated rabbit aortic strip preparation. Intravenous bolus administration of Defibrotide at 5-50 mg/kg did not produce any changes in the mean arterial blood pressure up to 3 hours. Defibrotide treated rabbits also resisted human serum-stasis and stasis alone induced venous and arterial thrombus formation. Serum and plasma from Defibrotide treated animals were tested for their direct contractile and procontractile (synergistic with an epinephrine stimulus) activities on rabbit aortic strips. In contrast to plasma and serum from saline treated rabbits, both serum and plasma produced relatively weak or no effects. The dose-contrac-tion responses were shifted to the right suggesting that serum from Defibrotide treated animals contained much lesser amounts of contractile substances. This data indicates blood from Defibrotide treated rabbits is compositionally different than normal, either due to lack of cellular product formation (thromboxane B 2, serotonin) or due to the generation of endothelial products which are inhibitory to the contractile effects of substances generated during the formation of a thrombus. Plasma thromboxane B2/6 keto-PGFia ratios were also found to be much higher in Defibrotide treated groups when compared to the saline groups. The observed therapeutic effect of Defibrotide in acute myocardial infarction may be linked with the inhibition of the formation of thrombus and with the mediation of vascular spasm due to the generation of inhibitory substances or the lack of generation of spasmogenic substances.
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Senhorinha, Gláucia Maria, Arlys Emanuel Mendes da Silva Santos, and Douglas Daniel Dophine. "The role of metabolic syndrome in Alzheimer’s disease." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.319.

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Background: Metabolic syndrome (MS) leads to the deposits formation of insoluble protein aggregates, neuroinflammation, oxidative stress, neuronal insulin resistance, progressive insulin resistance, desensitization and β-amyloid amyloidosis in the brain, besides direct ischemic effects which are closely associated with Alzheimer’s disease (AD).1 Objectives: The present study seeks to understand the role of the metabolic syndrome in the pathophysiology of Alzheimer’s disease and to describe preventive and therapeutic interventions. Methods: PUBMED and Web of Science were the databases used, the following descriptors were used to search the articles: “Alzheimer Disease” OR “Alzheimer Dementia” AND “Metabolic Syndrome”. Results: The studies in general have shown that MS is related to AD through brain insulin resistance, triggered by oxidative stress and neuroinflammation. It is related to the progressive atrophy of brain regions involved in the progression of AD. Insulin resistance in the brain is related to the progressive atrophy of the brain regions from initial progression of AD. These regions are cingulate cortices, medial temporal lobe, prefrontal gyri and other regions.³ Thus, there is an inhibition of the mechanisms of beta-amyloid removal, leading to its accumulation, which generates neuroinflammation, that in turn potentiates insulin resistance in the central nervous system, contributing to the genesis and progression of cognitive damage.2,3 Conclusions: Insulin resistance plays a major role in the initiation and perpetuation of cognitive impairment in AD. Furthermore, the components of the MS associated with AD, when treated with preventive and therapeutic measures, break this association by promoting rebalancing of the metabolism.
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