Gotowe bibliografie tematyczne / Ischaemia-reperfusion

Gotowa bibliografia na temat „Ischaemia-reperfusion”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 20 lutego 2023

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Artykuły w czasopismach na temat "Ischaemia-reperfusion"

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Kotsis, T. E., i P. B. Dimakakos. "Ischaemia/Reperfusion". European Journal of Vascular and Endovascular Surgery 22, nr 2 (sierpień 2001): 186–87. http://dx.doi.org/10.1053/ejvs.2001.1427.

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Zhang, Pei-Lei, Hai-Tao Lu, Jun-Gong Zhao i Ming-Hua Li. "Protective effect of dl-3n-butylphthalide preconditioning on focal cerebral ischaemia-reperfusion injury in rats". Acta Neuropsychiatrica 25, nr 1 (luty 2013): 12–17. http://dx.doi.org/10.1111/j.1601-5215.2012.00649.x.

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ObjectiveTo investigate the effect of dl-3n-butylphthalide (NBP) on the protection of cerebral tissue and possible mechanism on ischaemia-reperfusion injury, and to find out whether NBP therapy can extend the reperfusion window in an experimental stroke model in rats.MethodsSeventy-two Sprague-Dawley rats were randomly divided into sham operation, ischaemia-reperfusion and ischaemia-reperfusion with NBP groups. Focal cerebral ischaemia was induced using the modified intraluminal thread method and maintained for 2, 3 or 4 h. The ischaemia-reperfusion group received reperfusion immediately after ischaemia-reperfusion. The NBP group received intraperitoneal injection of NBP immediately after ischaemia, followed by reperfusion. The sham operation group received only injection of physiological saline. The cerebral infarction volume and neurological deficit were analysed, and vascular endothelial growth factor (VEGF) expression in brain tissues was visualised by immunohistochemistry.ResultsNBP treatment caused a significant decrease in both infarction volume and neurological deficit compared with the ischaemia-reperfusion group at corresponding time points in each (p < 0.05). In the NBP group, the infarction volume and neurological deficit did not change with different ischaemia times. The expression of VEGF was significantly decreased in the ischaemia-reperfusion group compared with the sham group (p < 0.01), while this change was partly prevented in the NBP group (p < 0.01). The expression of VEGF in brain tissue in both the NBP and ischaemia-reperfusion groups gradually decreased when the ischaemic period was prolonged.ConclusionNBP treatment has a protective effect against cerebral ischaemia; this possible mechanism maybe related to the VEGF expression and may extend the reperfusion window for subsequent salvage of cerebral ischaemia by reperfusion.
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Huber, Thomas. "Ischaemia-reperfusion injury". Journal of Vascular Surgery 31, nr 5 (maj 2000): 1081–82. http://dx.doi.org/10.1067/mva.2000.105513.

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Olds, Robin. "Ischaemia–reperfusion injury". Pathology 31, nr 4 (1999): 444. http://dx.doi.org/10.1016/s0031-3025(16)34766-3.

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McIntyre, Kenneth E. "ISCHAEMIA-REPERFUSION INJURY". Shock 12, nr 3 (wrzesień 1999): 246. http://dx.doi.org/10.1097/00024382-199909000-00019.

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AL-QATTAN, M. M. "Ischaemia-Reperfusion Injury". Journal of Hand Surgery 23, nr 5 (październik 1998): 570–73. http://dx.doi.org/10.1016/s0266-7681(98)80003-x.

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Prolonged ischaemia sometimes occurs in replantation and free flap surgery. The re-establishment of circulatory flow to the ischaemic tissue leads to a cascade of events which augments tissue necrosis. This paper reviews the pathophysiology of this ischaemia-reperfusion injury and discusses different methods to modulate this injury.
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Grace, P. A. "Ischaemia-reperfusion injury". British Journal of Surgery 81, nr 5 (maj 1994): 637–47. http://dx.doi.org/10.1002/bjs.1800810504.

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Westman, Bo, Anders Thörne, Olav Rooyackers, Katarina Fredriksson, Jan Wernerman i Folke Hammarqvist. "Glutathione and amino acid concentrations in human liver during short warm ischaemia and reperfusion: a pilot study". Clinical Science 117, nr 9 (1.09.2009): 339–44. http://dx.doi.org/10.1042/cs20080654.

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Glutathione is a major antioxidant, and, in the present study, we investigated whether a clinical model of short warm ischaemia and reperfusion of the human liver during surgery would influence glutathione and amino acid metabolism. Previous studies in humans have demonstrated that ischaemia and reperfusion in skeletal muscle for up to 120 min have no major effect on muscle glutathione concentrations. Liver ischaemia and reperfusion in animals have demonstrated diverging results concerning glutathione metabolism. In the present study, six patients with liver malignancies, undergoing liver resection during warm ischaemia, were included. Liver biopsies were obtained from healthy appearing liver tissue from both lobes before ischaemia and at maximal ischaemia, and from the remaining liver lobe after 5, 10, 15, 20, 25 and 30 min of reperfusion. The biopsies were analysed for glutathione, amino acids and lactate. Median ischaemia time was 28 (range, 15–36) min. Lactate increased 266% at maximal ischaemia (P<0.05). No alterations in glutathione concentrations or the redox status of glutathione (GSH/total glutathione) were observed. Glutamate decreased 22% (P<0.05) at maximal ischaemia and increased thereafter 72% at 30 min of reperfusion (P<0.05). Alanine increased 105% at maximal ischaemia (P<0.05) and was normalized during reperfusion. BCAAs (branched-chain amino acids) increased 67% at maximal ischaemia (P<0.05). In conclusion, short-time ischaemia and reperfusion in the human liver did not affect glutathione concentrations, whereas changes were observed in amino acid concentrations during both ischaemia and reperfusion.
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BÖHM, Felix, Magnus SETTERGREN, Adrian T. GONON i John PERNOW. "The endothelin-1 receptor antagonist bosentan protects against ischaemia/reperfusion-induced endothelial dysfunction in humans". Clinical Science 108, nr 4 (22.03.2005): 357–63. http://dx.doi.org/10.1042/cs20040317.

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Endothelial dysfunction may contribute to the extent of ischaemia/reperfusion injury. ET (endothelin)-1 receptor antagonism protects against myocardial ischaemia/reperfusion injury in animal models. The present study investigated whether oral administration of an ETA/ETB receptor antagonist protects against ischaemia/reperfusion-induced endothelial dysfunction in humans. FBF (forearm blood flow) was measured with venous occlusion plethysmography in 13 healthy male subjects. Forearm ischaemia was induced for 20 min followed by 60 min of reperfusion. Using a cross-over protocol, the subjects were randomized to oral administration of 500 mg of bosentan or placebo 2 h before ischaemia. Endothelium-dependent and -independent vasodilatation were determined by intra-brachial infusion of acetylcholine (1–10 μg/min) and nitroprusside (0.3–3 μg/min) respectively, before and after ischaemia. Compared with pre-ischaemia, the endothelium-dependent increase in FBF was significantly impaired at 15 and 30 min of reperfusion when the subjects received placebo (P<0.01). When the subjects received bosentan, the endothelium-dependent increase in FBF was not affected by ischaemia/reperfusion. Endothelium-independent vasodilatation was not affected during reperfusion compared with pre-ischaemia. The vaso-constrictor response induced by intra-arterial infusion of ET-1 was attenuated significantly by bosentan (P<0.001). The results suggest that the dual ETA/ETB receptor antagonist bosentan attenuates ischaemia/reperfusion-induced endothelial dysfunction in humans in vivo. Bosentan may thus be a feasible therapeutic agent in the treatment of ischaemia/reperfusion injury in humans.
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Bibli, Sofia-Iris, Eleni V. Toli, Agapi D. Vilaeti, Varnavas C. Varnavas, Giannis G. Baltogiannis, Apostolos Papalois, Zenon S. Kyriakides i Theofilos M. Kolettis. "Endothelin-B Receptors and Left Ventricular Dysfunction after Regional versus Global Ischaemia-Reperfusion in Rat Hearts". Cardiology Research and Practice 2012 (2012): 1–9. http://dx.doi.org/10.1155/2012/986813.

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Background. Endothelin-1 (ET-1) is implicated in left ventricular dysfunction after ischaemia-reperfusion. ETA and ETB receptors mediate diverse actions, but it is unknown whether these actions depend on ischaemia type and duration. We investigated the role of ETB receptors after four ischaemia-reperfusion protocols in isolated rat hearts.Methods. Left ventricular haemodynamic variables were measured in the Langendorff-perfused model after 40- and 20-minute regional or global ischaemia, followed by 30-minute reperfusion. Wild-type (n=39) and ETB-deficient (n=41) rats were compared. Infarct size was measured using fluorescent microspheres after regional ischaemia-reperfusion.Results. Left ventricular dysfunction was more prominent in ETB-deficient rats, particularly after regional ischaemia. Infarct size was smaller (P=0.006) in wild-type (31.5±4.4%) than ETB-deficient (45.0±7.3%) rats after 40 minutes of regional ischaemia-reperfusion. Although the recovery of left ventricular function was poorer after 40-minute ischaemia-reperfusion, end-diastolic pressure in ETB-deficient rats was higher after 20 than after 40 minutes of regional ischaemia-reperfusion.Conclusion. ETB receptors exert cytoprotective effects in the rat heart, mainly after regional ischaemia-reperfusion. Longer periods of ischaemia suppress the recovery of left ventricular function after reperfusion, but the role of ETB receptors may be more important during the early phases.
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Rozprawy doktorskie na temat "Ischaemia-reperfusion"

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Mankad, Pankaj Shashikant. "Ischaemia-reperfusion injury and endothelial dysfunction". Thesis, Imperial College London, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.392286.

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Koo, Dicken D. H. "Ischaemia/reperfusion injury in renal transplantation". Thesis, University of Oxford, 1999. http://ora.ox.ac.uk/objects/uuid:e0177fd9-1504-4c76-b9fd-6e7ae0b6b466.

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Kidney transplants from both living-related (LRD) and living unrelated (LURD) donors have superior function and survival than transplants from cadaver donors. This may be unsurprising as kidneys from living donors are procured under optimal conditions, from healthy donors with minimal ischaemia times. In contrast, cadaver kidneys are obtained from traumatised donors and may experience extended periods of cold ischaemic storage before transplantation. An immunohistochemical analysis has been performed on biopsies obtained before, and immediately after transplantation, to investigate the potential causes of early inflammatory events associated with cadaver renal transplantation that may influence subsequent graft outcome. An immunohistochemical analysis of biopsies obtained before transplantation demonstrated upregulated expression of endothelial E-selectin and proximal tubular expression of ICAM-1, VCAM-1 and HLA Class II antigens in cadaver donor kidneys. Analysis of donor parameters demonstrated that traumatic physiological events experienced in intensive care around the time of brain death were significantly associated with the induction of proinflammatory antigens. Antigen induction in cadaver donor kidneys before transplantation was significantly associated with early acute rejection. Furthermore, in cadaveric kidneys with long cold ischaemia times, glomerular neutrophil infiltration and deposition of activated platelets expressing P-selectin on intertubular capillaries were detected following reperfusion, in association with impaired short and long term graft function. Expression of inflammatory mediators were absent in all LRD renal allografts before and after reperfusion. A clinical trial was performed to determine whether ischaemia/reperfusion injury may be ameliorated by reflushing cadaver kidneys after cold storage to remove harmful products that may have accumulated in the vessel lumen. Reflushing did not prevent the inflammatory events observed after reperfusion or improve graft function. Therefore, a novel, oxygen free radical scavenger (lec-SOD) was obtained to assess its potential efficacy in preventing ischaemia/reperfusion injury. Lec-SOD bound with high affinity to macro- and microvascular endothelial cells under cold hypoxic conditions following incorporation into Marshall's preservation solution, significantly inhibiting cold hypoxia induced cell death, adhesion molecule induction and neutrophil adhesion. Furthermore, preservation of kidneys with lec- SOD for 18 hr in an experimental model of chronic renal allograft rejection, significantly attenuated neutrophil infiltration and MHC Class I induction day 1 post-transplant, with improved long term renal function. The results presented in this Thesis demonstrate that donor factors and cold ischaemia/ reperfusion injury elicit an early inflammatory response that may influence graft outcome of cadaver kidneys. Refinements in donor management and organ preservation may limit the deleterious effects of ischaemia/reperfusion injury in cadaver renal allografts, increasing graft survival to that observed in living donor transplantation.
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Cartaya, Rafael Eduardo Chavez. "Study on liver ischaemia and reperfusion". Thesis, University of Cambridge, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.388665.

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Fitridge, Robert Alwyn. "Reperfusion injury in focal cerebral ischaemia /". Title page, table of contents and abstract only, 1995. http://web4.library.adelaide.edu.au/theses/09MS/09msf546.pdf.

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Thummachote, Mr Yongsuk. "The pathopysiological consequence of ischaemia reperfusion injury". Thesis, University of London, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.498481.

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Kinross, James M. "Systems metabolism of intestinal ischaemia/reperfusion injury". Thesis, Imperial College London, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.543342.

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Sheth, H. "Therapeutic modulation of liver ischaemia reperfusion injury". Thesis, University College London (University of London), 2011. http://discovery.ucl.ac.uk/1318134/.

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Liver Ischaemia Reperfusion Injury (IRI) leads to production of reactive oxygen species and cytokines, which affects hepatocellular function following liver resection and transplantation. This thesis examines 2 hypotheses: 1) The role of intravenous glycine in amelioration of liver IRI in a in vivo animal model of partial lobar liver IRI. 2) Does prophylactically administered N-acetylcysteine prevent liver IRI in patients undergoing elective liver resection. Materials and Methods 1) A rabbit model of hepatic lobar IRI was used to evaluate glycine. 3 groups (n=6) Sham group (laparotomy alone), ischaemia reperfusion (I/R) group (1 hour ischaemia and 6 hours of reperfusion), and glycine I/R group (IV glycine 5 mg/kg prior to the I/R protocol) were used. Portal blood flow, bile flow and bile was analysed by H1NMR spectroscopy. Hepatic microcirculation, intracellular tissue oxygenation, serum TNFα, IL-8, ALT, AST were measured at 1, 2, 4 and 6 hours following reperfusion. 2) A randomised double blind clinical trial was conducted to assess the effect of NAC on liver IRI following liver resections. The main outcomes were: morbidity and mortality, ICAM-1 expression in liver tissue, liver function tests. Patients were randomised to receive NAC as IV infusion (NACG) or a placebo group (PG) which received 5% dextrose only. Immunohistochemistry for ICAM-1 was carried out on perioperative liver biopsies. Results 1) Glycine normalised the bile flow, reduced phosphatidylcholine shedding, lactate surge, and stimulated bile acid, pyruvate, glucose and acetoacetate release. Glycine improved portal blood flow, hepatic microcirculation by the 2nd hour, and hepatic intracellular tissue oxygenation by the 4th hour of reperfusion. Glycine ameliorated serum TNFα at 1, 2 and 4 hours and serum Il- 8, AST and ALT up to 6 hours post reperfusion as compared to the I/R alone group. 2) Of the 43 patients, 15 received NAC, 16 were randomised to the PG, 12 were excluded due to inoperable tumours. Serum ALT was reduced in NACG (p=0.001), while serum ALP was higher in the NACG (p=0.003). ICAM-1 expression was up-regulated in 6/16 patients in the PG and in 3/15 patients in NACG. ICAM-1 was down-regulated in 1/15 patients in the NACG and none in the PG, the difference was not significant. Conclusions 1) Glycine ameliorated liver IRI, improved bile flow and composition. 2) NAC ameliorated parenchymal liver injury and enhanced liver regeneration in patients undergoing elective liver resection.
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Laight, David W. "Neutrophils and vascular reactivity in ischaemia/reperfusion". Thesis, University of Bath, 1994. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.385291.

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Mokhtarudin, Mohd Jamil Mohamed. "Mathematical modelling of cerebral ischaemia-reperfusion injury". Thesis, University of Oxford, 2016. http://ora.ox.ac.uk/objects/uuid:3f5dd7cf-e403-4cf0-b725-4ac235c1b37e.

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Restoring cerebral blood flow using reperfusion treatment is a common method in treating ischaemic stroke. Reperfusion treatment should be given within 4.5 hours from stroke onset. However, reperfusion beyond this time window poses the risk of reperfusion injuries such as intracranial haemorrhage and cerebral tissue swelling. The focus of this thesis is to study the effect of cerebral tissue swelling after reperfusion as it can occur in a few hours after the treatment. Cerebral tissue swelling may cause brain structure movement and cerebral microvessel compression; the latter may then lead to secondary ischaemia occurrence. In this thesis, two mathematical models are presented. The first model investigates the effect of ischaemia-reperfusion in the formation of cerebral tissue swelling. This model provides the understanding of suitable reperfusion conditions to reduce the effect of tissue swelling and also becomes the basis for the subsequent model. Meanwhile, the second model studies the role of a water-transporting protein, aquaporin-4 in ischaemia-reperfusion and its potential as part of treatments for cerebral tissue swelling. In addition, the ionic concentration may change during ischaemia which may be a factor contributing to cerebral tissue swelling. Thus, the effect of ionic concentration on the swelling formation is also investigated. Finally, validations of these models are achieved by developing patient-specific geometries from available ischaemic stroke patient MRI data and utilising finite element analysis. Comparison between the simulation results and the MRI data is done by quantifying the brain ventricles movement during cerebral tissue swelling.
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Vejchapipat, Paisarn. "Intestinal and hepatic metabolism after intestinal ischaemia reperfusion". Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.248437.

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Książki na temat "Ischaemia-reperfusion"

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A, Grace P., i Mathie Robert T, red. Ischaemia reperfusion injury. Oxford: Blackwell Science, 1999.

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Khaira, Harmeet Singh. Ischaemia-reperfusion in intermittent claudication. Birmingham: University of Birmingham, 1995.

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Wilson, Ian Clark. The role of leucocytes in neonatal myocardial ischaemia-reperfusion injury. Birmingham: University of Birmingham, 1994.

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Herman, Stanley Leon. Age differences in the susceptibility of the normal rabbit myocardium to injury following ischaemia and reperfusion. Ottawa: National Library of Canada, 1992.

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Alfred Benzon Symposium (41st 1996 Royal Danish Academy of Sciences and Letters). Coronary microcirculation during ischaemia and reperfusion: Proceedings of a symposium held at the Royal Danish Academy of Sciences and Letters, August 18-22, 1996. Redaktorzy Aldershvile Jan, Haunsø Stig i Svendsen Jesper Hastrup. Copenhagen: Munksgaard, 1997.

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Haunso. Coronary Microcirculation During Ischaemia & Reperfusion. Blackwell Science Inc, 1997.

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Fink, Mitchell P. Ischaemia-reperfusion injury in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0308.

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Ischaemia/reperfusion (I/R) injury contributes to the pathogenesis of many common clinical conditions, including stroke, myocardial damage after percutaneous intervention for acute coronary artery occlusion, primary graft dysfunction after solid organ transplantation. The mechanisms that are responsible for I/R injury remain incompletely understood, but damage caused by reactive oxygen species (ROS) and reactive nitrogen species clearly is important. A number of therapeutic approaches, such as administration of ROS scavengers, are effective in animal models of I/R injury, but for the most part, translation of these findings into strategies that can clearly benefit patients has yet to be achieved.
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Hausenloy, Derek, i Derek Yellon, red. An Introduction to Cardioprotection. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199544769.003.0001.

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• In its broadest sense, the term ‘cardioprotection’ encompasses ‘all mechanisms and means that contribute to the preservation of the heart by reducing or even preventing myocardial damage’• However, for the purposes of this book, the term ‘cardioprotection’ will refer to the endogenous mechanisms and therapeutic strategies that reduce or prevent myocardial damage induced by acute ischaemia-reperfusion injury• In this context, cardioprotection begins with the primary prevention of coronary heart disease and includes the reduction of myocardial injury sustained during coronary artery bypass graft surgery, and an acute myocardial infarction, conditions with considerable morbidity and mortality• An understanding of the pathophysiology of acute myocardial ischaemia-reperfusion injury is essential when designing new cardioprotective strategies• Several methods exist for both quantifying myocardial damage induced by acute ischaemia-reperfusion injury and for assessing myocardial salvage following the application of cardioprotective strategies• Importantly, novel cardioprotective strategies must be capable of preventing and reducing myocardial damage over and above that provided by current optimal therapy.
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Downey, James, i Michael Cohen. Endogenous Mechanisms of Cardioprotection. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199544769.003.0008.

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• Ischaemic preconditioning is the most powerful endogenous mechanism for limiting myocardial infarct size in the experimental setting. Its clinical application is limited to scenarios in which the index episode of ischaemia and reperfusion can be anticipated such as in the setting of cardiac surgery• Ischaemic postconditioning represents an endogenous cardioprotective strategy which is applied at the onset of myocardial reperfusion, thereby allowing its use as an adjunct to reperfusion in patients presenting with an acute myocardial infarction• Both ischaemic preconditioning and postconditioning recruit a common signal transduction pathway at the time of myocardial reperfusion, which can be targeted by pharmacological agents administered as adjuncts to reperfusion.
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Jumean, Marwan F., i Mark S. Link. Post-cardiac arrest arrhythmias. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0065.

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Our understanding of arrhythmias following resuscitated cardiac arrest has evolved over the past two decades to entail complex pathophysiological processes including, in part, ischaemia and ischaemia-reperfusion injury. Electrical instability after the return of spontaneous circulation (ROSC) is common, ranging from atrial fibrillation to recurrent ventricular tachycardia and fibrillation. Electrical instability following out-of-hospital cardiac arrest is most commonly due to myocardial ischaemia and post-arrest myocardial dysfunction. However, electrolyte disturbances, elevated catecholamine levels, the frequent use of vasopressors and inotropes, and underlying structural heart disease or channelopathies also contribute in the acute setting. Limited data exists that specifically address the management of arrhythmias in the immediate post-arrest period. In addition to treating any potential reversible cause, the management in the haemodynamically-stable patient includes beta-blockers, class I (lignocaine and procainamide) and III anti-arrhythmic agents (amiodarone). Defibrillation is often needed for recurrent ventricular arrhythmias.
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Części książek na temat "Ischaemia-reperfusion"

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Froghi, Farid, Saied Froghi i Brian R. Davidson. "Liver Ischaemia-Reperfusion Injury". W Liver Diseases, 129–41. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-24432-3_12.

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Adembri, C., A. R. De Gaudio i G. P. Novelli. "Ischaemia-Reperfusion in Sepsis". W Sepsis and Organ Dysfunction, 49–56. Milano: Springer Milan, 2000. http://dx.doi.org/10.1007/978-88-470-2284-3_5.

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Lochner, A., E. Tromp i R. Mouton. "Signal transduction in myocardial ischaemia and reperfusion". W Biochemical Mechanisms in Heart Function, 129–36. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-1279-6_18.

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MacCarthy, P. A., i A. M. Shah. "The Role of Nitric Oxide in Cardiac Ischaemia-Reperfusion". W Nitric Oxide, 545–70. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-642-57077-3_22.

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Winn, Robert K., Sam R. Sharar, Nicholas B. Vedder i John M. Harlan. "Leukocyte and Endothelial Adhesion Molecules in Ischaemia/Reperfusion Injuries". W Ciba Foundation Symposium 189 - Cell Adhesion and Human Disease, 63–78. Chichester, UK: John Wiley & Sons, Ltd., 2007. http://dx.doi.org/10.1002/9780470514719.ch6.

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Kingston, Ross. "The Therapeutic Role of Taurine in Ischaemia-Reperfusion Injury". W Apoptosome, 283–304. Dordrecht: Springer Netherlands, 2009. http://dx.doi.org/10.1007/978-90-481-3415-1_15.

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Mayne, L. V. "Changes in Cardiac Gene Expression After Ischaemia and Reperfusion". W Delayed Preconditioning and Adaptive Cardioprotection, 111–33. Dordrecht: Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-011-5312-6_6.

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Ferrari, R., C. Ceconi, S. Curello, A. Cargnoni, F. De Giuli, G. M. Boffa i A. Albertini. "Role of Oxygen in Myocardial Ischaemia and Reperfusion Damage". W Developments in Cardiovascular Medicine, 91–107. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-1607-7_9.

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Ferrari, R., S. Curello, C. Ceconi, A. Cargnoni, E. Condorelli i A. Albertini. "Alterations of Glutathione Status during Myocardial Ischaemia and Reperfusion". W Oxygen Radicals in the Pathophysiology of Heart Disease, 145–60. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-1743-2_10.

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Sumeray, Mark S., i Derek M. Yellon. "Characterisation and validation of a murine model of global ischaemia-reperfusion injury". W Myocardial Ischemia and Reperfusion, 61–68. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-4979-6_8.

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Streszczenia konferencji na temat "Ischaemia-reperfusion"

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Panico, Karine, Giovanni Weber, Marcela S. Carneiro-Ramos i Jo�o Salinet. "Electrophysiological Effects on Renal Ischaemia/Reperfusion-Induced Cardiac Hypertrophy". W 2017 Computing in Cardiology Conference. Computing in Cardiology, 2017. http://dx.doi.org/10.22489/cinc.2017.301-394.

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Bhandal, J., A. Hussain, J. Buckley i H. Maddock. "P34 Adenosine a1 receptor activation can protect the myocardium from ischaemia reperfusion injury post reperfusion". W British Society for Cardiovascular Research, Autumn Meeting 2017 ‘Cardiac Metabolic Disorders and Mitochondrial Dysfunction’, 11–12 September 2017, University of Oxford. BMJ Publishing Group Ltd and British Cardiovascular Society, 2018. http://dx.doi.org/10.1136/heartjnl-2018-bscr.39.

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Dookun, Emily, Anna Walaszczyk, Rachael Redgrave, Simon Tual-Chalot, Oliver Yausep, Ioakim Spyridopoulos, Andrew Owens, Helen Arthur, Joao Passos i Gavin Richardson. "142 Accumulation of cardiomyocyte senescence following ischaemia-reperfusion injury (IRI); a potential therapeutic target?" W British Cardiovascular Society Annual Conference ‘High Performing Teams’, 4–6 June 2018, Manchester, UK. BMJ Publishing Group Ltd and British Cardiovascular Society, 2018. http://dx.doi.org/10.1136/heartjnl-2018-bcs.138.

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Lim, Ven Gee, Sapna Arjun, Robert Bell i Derek Yellon. "BS10 Canagliflozin, an SGLT2 inhibitor attenuates ischaemia/reperfusion injury in the non-diabetic heart". W British Cardiovascular Society Annual Conference ‘Digital Health Revolution’ 3–5 June 2019. BMJ Publishing Group Ltd and British Cardiovascular Society, 2019. http://dx.doi.org/10.1136/heartjnl-2019-bcs.174.

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Draganova, Lilia, Rachael Redgrave, Simon Tual-Chalot, Sarah Marsh, Helen Arthur i Ioakim Spyridopoulos. "BS31 The role of fractalkine and CX3CR1-expressing lymphocytes during myocardial ischaemia/reperfusion injury". W British Cardiovascular Society Annual Conference ‘Digital Health Revolution’ 3–5 June 2019. BMJ Publishing Group Ltd and British Cardiovascular Society, 2019. http://dx.doi.org/10.1136/heartjnl-2019-bcs.194.

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Platt, Esther, Francis Robertson, Andrew Hall, Alberto Quaglia i Brian Davidson. "P053 Investigation of the origin of serum neutrophil gelatinase associated lipocalin (NGAL) following liver ischaemia reperfusion and resultant acute kidney injury in mice". W Abstracts of the British Association for the Study of the Liver Annual Meeting, 22–24 November 2021. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2021. http://dx.doi.org/10.1136/gutjnl-2021-basl.62.

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