Artykuły w czasopismach: „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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Akbas, H., M. Ozden, M. Kanko, H. Maral, S. Bulbul, S. Yavuz, E. Ozker i T. Berki. "Protective Antioxidant Effects of Carvedilol in a Rat Model of Ischaemia-reperfusion Injury". Journal of International Medical Research 33, nr 5 (wrzesień 2005): 528–36. http://dx.doi.org/10.1177/147323000503300508.

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This study investigated the protective effects of carvedilol, a potent antioxidant, in a rat model of tourniquet-induced ischaemia-reperfusion injury of the hind limb. Thirty rats were divided equally into three groups: the control group (group 1) was only anaesthetized, without creating an ischaemia-reperfusion injury; group 2 was submitted to ischaemia (4 h), followed by a 2-h reperfusion period; and group 3 was pre-treated with carvedilol (2 mg/kg per day) for 10 days prior to ischaemia-reperfusion. Ischaemia-reperfusion produced a significant decrease in superoxide dismutase and glutathione peroxidase activities in the liver, lungs, muscle and serum compared with control treatment, and pre-treatment with carvedilol prevented these changes. Ischaemia-reperfusion caused a significant increase in malondialdehyde and nitric oxide (NO) levels in liver, lungs, muscle (except NO) and serum compared with control treatment, and carvedilol prevented these changes. In conclusion, it might be inferred that carvedilol could be used safely to prevent oxidative injury during reperfusion following ischaemia in humans.

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Tak, Eunyoung, Gil-Chun Park, Seok-Hwan Kim, Dae Young Jun, Jooyoung Lee, Shin Hwang, Gi-Won Song i Sung-Gyu Lee. "Epigallocatechin-3-gallate protects against hepatic ischaemia–reperfusion injury by reducing oxidative stress and apoptotic cell death". Journal of International Medical Research 44, nr 6 (2.11.2016): 1248–62. http://dx.doi.org/10.1177/0300060516662735.

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Objective To investigate the protective effects of epigallocatechin-3-gallate (EGCG), a major polyphenol source in green tea, against hepatic ischaemia–reperfusion injury in mice. Methods The partial hepatic ischaemia–reperfusion injury model was created by employing the hanging-weight method in C57BL/6 male mice. EGCG (50 mg/kg) was administered via an intraperitoneal injection 45 min before performing the reperfusion. A number of markers of inflammation, oxidative stress, apoptosis and liver injury were measured after the ischaemia–reperfusion injury had been induced. Results The treatment groups were: sham-operated (Sham, n = 10), hepatic ischaemia–reperfusion injury (IR, n = 10), and EGCG with ischaemia–reperfusion injury (EGCG-treated IR, n = 10). Hepatic ischaemia–reperfusion injury increased the levels of biochemical and histological markers of liver injury, increased the levels of malondialdehyde, reduced the glutathione/oxidized glutathione ratio, increased the levels of oxidative stress and lipid peroxidation markers, decreased B-cell lymphoma 2 levels, and increased the levels of Bax, cytochrome c, cleaved caspase-3, and cleaved caspase-9. Pretreatment with EGCG ameliorated all of these changes. Conclusion The antioxidant and antiapoptotic effects of EGCG protected against hepatic ischaemia–reperfusion injury in mice.

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Dart, A. M., i R. A. Riemersma. "Origins of endogenous noradrenaline overflow during reperfusion of the ischaemic rat heart". Clinical Science 74, nr 3 (1.03.1988): 269–74. http://dx.doi.org/10.1042/cs0740269.

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1. Reperfusion of the globally ischaemic isolated rat heart is associated with an enhanced overflow of endogenous noradrenaline (NA) after ischaemic periods of 20, 40 or 60 min but not of 10 min. 2. Reperfusion NA overflow, after 40 min of ischaemia, is suppressed by desipramine and increased when ischaemia follows a period of substrate deprivation. 3. Reperfusion after 40 min of ischaemia is associated with a significant rise in NA concentration despite a simultaneous 20-fold increase in flow. This increase in concentration is abolished by treatment with desipramine or if ischaemia follows a period of substrate deprivation. 4. Reperfusion NA overflow correlates with the reperfusion overflow of an extracellular space marker infused before the ischaemic episode. 5. These results suggest that ischaemia is heterogeneous and that NA is released into regions of particularly profound ischaemia from which it is subsequently eluted during reperfusion.

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Ozkisacik, Sezen, Ali Onur Erdem, Barlas Etensel, Canten Tataroglu, Mukadder Serter i Mesut Yazici. "Short-interval postconditioning protects the bowel against ischaemia–reperfusion injury in rats". Journal of International Medical Research 45, nr 3 (28.05.2017): 1036–41. http://dx.doi.org/10.1177/0300060517708921.

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Objective Acute mesenteric ischaemia leads to intestinal damage. Restoration of blood flow results in further damage to tissue, which is called reperfusion injury. This study aimed to investigate the protective effects of short-interval postconditioning and to determine the optimal interval for reperfusion in an experimental rat model of intestinal ischaemia. Methods Forty adult male Wistar rats were grouped as follows: sham (Sh), ischaemia + reperfusion (IR), ischaemia + postconditioning for 5 seconds (PC5), ischaemia + postconditioning for 10 seconds (PC10), and ischaemia + postconditioning for 20 seconds (PC20). For postconditioning, 10 cycles of reperfusion (5, 10, or 20 seconds) interspersed by 10 cycles of 10 seconds of ischaemia were performed. Blood glutathione reductase (GR) and glutathione peroxidase (GPx) levels were measured. Intestinal tissue damage was assessed histopathologically. Results GR levels were significantly higher in the PC5 group than in the IR group (37.7 ± 9.0 vs. 18.5 ± 2.0 min/g Hb). GPx levels were significantly higher in the PC10 group than in the IR group (43.2 ± 9.2 vs. 15.9 ± 4.6 U/g Hb). The histopathological score was significantly lower in the PC5 group (1.1 ± 0.1) than in the IR group (2.1 ± 0.2). Conclusion Short-interval postconditioning reduces reperfusion injury in the ischaemic bowel and the optimal interval for reperfusion is 5 seconds. The long-term effects of short-interval postconditioning and the optimal reperfusion interval in intestinal ischaemia–reperfusion in rats need to be investigated.

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Khaliulin, Igor, Raimondo Ascione, Leonid N. Maslov, Haitham Amal i M. Saadeh Suleiman. "Preconditioning or Postconditioning with 8-Br-cAMP-AM Protects the Heart against Regional Ischemia and Reperfusion: A Role for Mitochondrial Permeability Transition". Cells 10, nr 5 (17.05.2021): 1223. http://dx.doi.org/10.3390/cells10051223.

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The cAMP analogue 8-Br-cAMP-AM (8-Br) confers marked protection against global ischaemia/reperfusion of isolated perfused heart. We tested the hypothesis that 8-Br is also protective under clinically relevant conditions (regional ischaemia) when applied either before ischemia or at the beginning of reperfusion, and this effect is associated with the mitochondrial permeability transition pore (MPTP). 8-Br (10 μM) was administered to Langendorff-perfused rat hearts for 5 min either before or at the end of 30 min regional ischaemia. Ca2+-induced mitochondria swelling (a measure of MPTP opening) and binding of hexokinase II (HKII) to mitochondria were assessed following the drug treatment at preischaemia. Haemodynamic function and ventricular arrhythmias were monitored during ischaemia and 2 h reperfusion. Infarct size was evaluated at the end of reperfusion. 8-Br administered before ischaemia attenuated ventricular arrhythmias, improved haemodynamic function, and reduced infarct size during ischaemia/reperfusion. Application of 8-Br at the end of ischaemia protected the heart during reperfusion. 8-Br promoted binding of HKII to the mitochondria and reduced Ca2+-induced mitochondria swelling. Thus, 8-Br protects the heart when administered before regional ischaemia or at the beginning of reperfusion. This effect is associated with inhibition of MPTP via binding of HKII to mitochondria, which may underlie the protective mechanism.

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VÁGÓ, Hajnalka, Pál SOÓS, Endre ZIMA, László GELLÉR, Violetta KÉKESI, Terézia ANDRÁSI, Tamás SZABÓ, Alexander Juhász-Nagy i Béla MERKELY. "The ETA receptor antagonist LU 135252 has no electrophysiological or anti-arrhythmic effects during myocardial ischaemia/reperfusion in dogs". Clinical Science 103, s2002 (1.09.2002): 223S—227S. http://dx.doi.org/10.1042/cs103s223s.

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The anti-arrhythmic effects of ETA receptor antagonists during myocardial ischaemia and reperfusion remain controversial. Moreover, the electrophysiological mechanism has not yet been identified. The aim of this study was to investigate the potential anti-arrhythmic and electrophysiological effects of the ETA receptor antagonist LU 135252 (LU) during myocardial ischaemia and reperfusion in a canine model. A bolus of LU (1mg/kg; n = 10) or saline (control; n = 10) was injected into the left anterior descending coronary artery before ligation of this vessel for 30min, which was followed by a 90-min reperfusion period. LU bolus administration (0.5mg/kg) was repeated every 30min. There were no differences in mean arterial blood pressure or coronary blood flow between the two groups. The determined left ventricular ischaemic mass was 25.5±1.8% and 27.8±2.2% of the total left ventricular mass in the control and LU groups respectively. The total incidence of ventricular fibrillation during ischaemia and reperfusion was 40% in the control and 50% in the LU group (not significantly different). The incidence of non-sustained and sustained ventricular tachycardias during ischaemia, reperfusion and over the whole period (ischaemia plus reperfusion) in the control group was 50%, 50% and 70% respectively, and that in the LU group was 80%, 70% and 100% respectively (no significant differences between groups). The number of ventricular premature beats was not decreased by LU during either ischaemia or reperfusion [median (25th–75th percentile): ischaemia, 20 (13–37) and 56 (32–130) for LU and control groups respectively; reperfusion, 15 (2–21) and 39 (7–74) respectively; ischaemia+reperfusion, 16 (4–35) and 43 (10–82) respectively; no significant differences between groups]. During ischaemia, the monophasic action potential duration at 90% repolarization (MAPD90) decreased significantly, while during reperfusion a significant prolongation of MAPD90 was observed in the left anterior descending region that was similar in the two groups. In conclusion, LU did not affect repolarization changes and did not have anti-arrhythmic effects during either ischaemia or reperfusion in this model.

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Mangino, M. J., M. Murphy, A. Bohrer i J. Turk. "Platelet Activating Factor Synthesis and Metabolism in Intestinal Ischaemia-Reperfusion Injury". Mediators of Inflammation 3, nr 5 (1994): 393–95. http://dx.doi.org/10.1155/s0962935194000554.

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The object of this study was to characterize the synthesis and metabolism of platelet activating factor (PAF) by intestinal mucosa subjected to ischaemia–reperfusion injury. Canine intestinal mucosa produced 16:0-PAF, 18:0-PAF, and high levels of the corresponding lyso- PAF metabolites. Three h of intestinal ischaemia and ischaemia followed by 1 h of reperfusion did not affect the synthesis or metabolism of PAF by intestinal mucosa. Intestinal mucosa elaborated a factor that rapidly hydrolyzes PAF to lyso-PAF. The observed hydrolysis rate was not altered by ischaemia or ischaemia and reperfusion. In conclusion, this study suggests that intestinal mucosa produces PAF and rapidly hydrolyzes PAF. The PAF synthesis and metabolism rates of intestinal mucosa is not altered by ischaemia reperfusion in this model under the imposed conditions.

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SHYU, Kou-Gi, Chih-Chuan CHANG, Bao-Wei WANG, Peiliang KUAN i Hang CHANG. "Increased expression of angiopoietin-2 and Tie2 receptor in a rat model of myocardial ischaemia/reperfusion". Clinical Science 105, nr 3 (1.09.2003): 287–94. http://dx.doi.org/10.1042/cs20030025.

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The angiopoietins and Tie receptors are involved in blood vessel formation. The role of the angiopoietin/Tie receptor system in myocardial ischaemia/reperfusion is not well known. To investigate the participation of angiopoietins and Tie receptors in myocardial ischaemia/reperfusion, adult Wistar rats were studied in which the left coronary artery was ligated for 30 min, followed by reperfusion. Angiopoietin-1 (Ang1), angiopoietin-2 (Ang2), Tie1 and Tie2 were measured immediately after relief of occlusion, and 1, 6, 24 and 72 h after reperfusion, by Northern blot, Western blot and immunohistochemical staining. Ang2 mRNA was increased significantly at 24 h and 48 h after reperfusion, and returned to baseline levels at 72 h, in the jeopardized myocardium. Tie2 mRNA increased 3.4-fold immediately after the relief of occlusion, reached a maximum 8-fold increase at 24 h after reperfusion and remained elevated up to 72 h. Ang2 protein levels also increased after reperfusion, reaching a maximum 2.2-fold increase at 48 h after reperfusion. Tie2 protein increased immediately after relief of ischaemia, and showed a significant increase from 6 h to 72 h after reperfusion as compared with the sham control. Ang1 and Tie1 mRNA and protein did not show significant changes after ischaemia/reperfusion. Immunohistochemical studies also showed increased immunoreactivity of Ang2 and Tie2 in the jeopardized myocardium after ischaemia/reperfusion. In conclusion, expression of both Ang2 and Tie2 increased after ischaemia/reperfusion in the rat ventricular myocardium, while the expression of Ang1 and Tie1 did not.

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Weight, S. C., P. R. F. Bell i M. L. Nicholson. "Renal ischaemia-reperfusion injury". British Journal of Surgery 83, nr 2 (luty 1996): 162–70. http://dx.doi.org/10.1046/j.1365-2168.1996.02182.x.

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Weight, S. C., P. R. F. Bell i M. L. Nicholson. "Renal ischaemia-reperfusion injury". British Journal of Surgery 83, nr 2 (luty 1996): 162–70. http://dx.doi.org/10.1002/bjs.1800830206.

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Westman, Bo, Lars Weidenhielm, Olav Rooyackers, Katarina Fredriksson, Jan Wernerman i Folke Hammarqvist. "Knee replacement surgery as a human clinical model of the effects of ischaemia/reperfusion upon skeletal muscle". Clinical Science 113, nr 7 (3.09.2007): 313–18. http://dx.doi.org/10.1042/cs20070025.

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The temporal pattern of metabolic alterations in muscle tissue during total ischaemia and reperfusion are not well-characterized in humans with respect to glutathione, amino acids and energy-rich compounds. In the present study, knee replacement surgery was used as a clinical model to elucidate this pattern of metabolic alterations. Patients (n=15) undergoing elective knee replacement surgery employing tourniquet ischaemia were studied. Muscle biopsies were taken from the quadriceps femoris muscle on the operated side preoperatively, at maximal ischaemia and after 24 h of reperfusion. The biopsies were analysed for glutathione, amino acids and energy-rich compounds. In addition the patients were randomized to receive either glucose or a mannitol infusion in the 24 h following tourniquet ischaemia. During ischaemia, muscle lactate increased by 400% (P<0.05) and phosphocreatine decreased by 70% (P<0.05). During the subsequent 24 h of reperfusion, muscle-reduced glutathione and total glutathione decreased by 27% and 22% (P<0.05) respectively. The muscle amino acid pattern changed during ischaemia with an increase in alanine by 65% (P<0.001) and a decrease in glutamate by 29% (P<0.001). During the reperfusion part of the study, no differences attributable to the infusion of mannitol or glucose were observed. During tourniquet ischaemia and subsequent reperfusion, changes in glutathione metabolism developed, indicating oxidative stress. Knee replacement surgery as a clinical model was useful during the ischaemia period, whereas the reperfusion period was dominated by the general changes seen postoperatively.

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Messent, M., M. J. D. Griffiths i T. W. Evans. "Pulmonary Vascular Reactivity and Ischaemia-Reperfusion Injury in the Rat". Clinical Science 85, nr 1 (1.07.1993): 71–75. http://dx.doi.org/10.1042/cs0850071.

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1. The endothelium has been shown to modulate the pulmonary vascular response to hypoxia in the rat. Acute lung injury is associated with loss of hypoxic pulmonary vasoconstriction and increased pulmonary vascular permeability. Similar loss of the vascular response to hypoxia is seen after ischaemia-reperfusion injury of the myocardium. 2. The effects of reperfusion injury on pulmonary endothelial integrity, as shown by the albumin escape index and hypoxic pulmonary vasoconstriction, were investigated in isolated, blood-perfused rat lungs. 3. Ischaemia for 0.5 h, which itself caused no increase in the albumin escape index, was followed by reperfusion for 0.25 h, 0.5 h and 1 h. Controls were subjected to 2 h of perfusion only (n = 5 in all groups). The pulmonary pressor response to hypoxia (fractional inspired oxygen concentration, 3%) was measured before and after ischaemia-reperfusion, and the dilator response to acetylcholine was measured after ischaemia-reperfusion in all cases. 4. Ischaemia-reperfusion significantly increased the albumin escape index after 0.5 h (mean ± SEM, 1.40 ± 0.27) and 1 h (2.0 ± 0.30) compared with controls (0.54 ± 0.30, P <0.05 in both cases). The pulmonary pressor response to hypoxia was augmented significantly after reperfusion when compared with baseline hypoxic pulmonary vasoconstriction (change from baseline: 13.2 ± 4.63 and 22.2 ± 7.1% after 0.5 and 1.0 h of reperfusion, respectively, P <0.05). Vasorelaxation of sustained hypoxic vasoconstriction using acetylcholine was similar in both control lungs and those subjected to ischaemia-reperfusion. 5. These results suggest that the pressor response to hypoxia is augmented after damage to the pulmonary vascular endothelium induced by ischaemia-reperfusion. Although this may be due to diminished release of endothelium-derived relaxing factors, the normal vasodilator response to acetylcholine suggests the phenomenon is not due to a reduction in the release of endothelium-derived relaxing factor/nitric oxide.

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Wiersema, A. M., R. Dirksen, W. J. G. Oyen i J. A. van der Vliet. "A method for long duration anaesthesia for a new hindlimb ischaemia-reperfusion model in mice". Laboratory Animals 31, nr 2 (1.04.1997): 151–56. http://dx.doi.org/10.1258/002367797780600125.

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To study the relationship between ischaemia-reperfusion and multiple organ dysfunction syndrome (MODS), a new anaesthesia method was required to be applied to C57BL/6 mice. These mice are also used in a well accepted, standardized model for MODS using intraperitoneally administered zymosan (zymosan induced general inflammation, ZIGI). The aim was to develop a new model for ischaemia-reperfusion with 6 h of anaesthesia. This and further specific requirements for the combination of ischaemia-reperfusion and the ZIGI method, made us select inhalational anaesthesia using isoflurane in oxygen. This study evaluates whether long-term anaesthesia confounds the results of ischaemia-reperfusion and the ZIGI model. In addition the benefits of using the analgesic buprenorphine were evaluated. Ischaemia was induced with a tourniquet around the hindlimb. Ischaemia and reperfusion were verified by imaging a radioactive tracer with a gamma-camera. It was established that anaesthesia with isoflurane in oxygen caused little perturbation of body temperature and respiratory rate. A survival rate of 89% without noteworthy influence on organs was obtained. Buprenorphine proved to provide adequate analgesia and had no influence on measured parameters. In our experimental setting, this model with long duration anaesthesia allowed us to induce ischaemia and reperfusion of the hindlimb without perturbation of measurements. It also allowed good exposure of the abdomen and facilitated combination with the ZIGI model.

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ZHANG, Jin-Gang, Sudip GHOSH, Colin D. OCKLEFORD i Manuel GALIÑANES. "Characterization of an in vitro model for the study of the short and prolonged effects of myocardial ischaemia and reperfusion in man". Clinical Science 99, nr 5 (27.10.2000): 443–53. http://dx.doi.org/10.1042/cs0990443.

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The mechanisms underlying myocardial ischaemia and reperfusion-induced injury have been investigated, mainly by using animal experimental preparations in vitro and in vivo, but little is known of the process in human myocardium. The present studies characterize an in vitro model using human myocardium for the study of early and delayed effects of ischaemia and reperfusion. The right atrial appendage was manually sliced and incubated in buffer through which was bubbled O2/CO2 (19:1, v/v) for various time periods. Lactate dehydrogenase (LDH) leakage, 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl-2H-tetrazolium bromide (MTT) reduction, oxygen consumption, nucleotide levels and tissue morphology were all investigated as markers of myocardial injury. The specimens remained stable and viable up to 24 h, but had significantly deteriorated by 48 h. The preparation responded to ischaemia in a time-related manner. Tissue viability was reduced by 25% after 30 min ischaemia, declined to 60% after 60 min ischaemia and to 75% after 120 min ischaemia. Interestingly, the tissue was more susceptible when ischaemia was induced after 24 h of aerobic incubation. The effects of the duration of reperfusion were investigated after a fixed 60 min ischaemic insult. The results of LDH leakage suggest that reperfusion injury is mainly sustained within the first 2 h of reperfusion. However, the results of MTT reduction show that there is a progressive decrease in tissue viability over the 24 h reperfusion period, possibly reflecting the occurrence of tissue necrosis and apoptosis at different reperfusion times. In conclusion, the data provide evidence that the incubation of human atrial tissue in vitro is stable, and slices are viable for at least 24 h, which permits the study of early and delayed consequences of ischaemia and reperfusion in the human myocardium.

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Gracia-Sancho, Jordi, Araní Casillas-Ramírez i Carmen Peralta. "Molecular pathways in protecting the liver from ischaemia/reperfusion injury: a 2015 update". Clinical Science 129, nr 4 (21.05.2015): 345–62. http://dx.doi.org/10.1042/cs20150223.

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

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Saeid, Feyzizadeh, Javadi Aniseh, Badalzadeh Reza i Vafaee S. Manouchehr. "Signaling mediators modulated by cardioprotective interventions in healthy and diabetic myocardium with ischaemia–reperfusion injury". European Journal of Preventive Cardiology 25, nr 14 (14.02.2018): 1463–81. http://dx.doi.org/10.1177/2047487318756420.

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

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Cabrera-Fuentes, Hector, Isabel Steinert, Klaus Preissner, Péter Bencsik, Márta Sárközy, Csaba Csonka, Péter Ferdinandy i in. "Mechanism and consequences of the shift in cardiac arginine metabolism following ischaemia and reperfusion in rats". Thrombosis and Haemostasis 113, nr 03 (maj 2015): 482–93. http://dx.doi.org/10.1160/th14-05-0477.

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SummaryCardiac ischaemia and reperfusion leads to irreversible injury and subsequent tissue remodelling. Initial reperfusion seems to shift arginine metabolism from nitric oxide (NO) to polyamine formation. This may limit functional recovery at reperfusion. The hypothesis was tested whether ischaemia/reperfusion translates such a shift in arginine metabolism in a tumour necrosis factor (TNF)-α-dependent way and renin-angiotensin system (RAS)-dependent way into a sustained effect. Both, the early post-ischaemic recovery and molecular adaptation to ischaemia/reperfusion were analysed in saline perfused rat hearts undergoing global no-flow ischaemia and reperfusion. Local TNF-α activation was blocked by inhibition of TNF-α sheddase ADAM17. To interfere with RAS captopril was administered. Arginase was inhibited by administration of Nor-NOHA. Long-term effects of ischemia/reperfusion on arginine metabolism were analysed in vivo in rats receiving an established ischaemia/reperfusion protocol in the closed chest mode. mRNA expression analysis indicated a shift in the arginine metabolism from NO formation to polyamine metabolism starting within 2 hours (h) of reperfusion and translated into protein expression within 24 h. Inhibition of the TNF-α pathway and captopril attenuated these delayed effects on post-ischaemic recovery. This shift in arginine metabolism was associated with functional impairment of hearts within 24 h. Inhibition of arginase but not that of TNF-α and RAS pathways improved functional recovery immediately. However, no benefit was observed after four months. In conclusion, this study identified TNF-α and RAS to be responsible for depressed cardiac function that occurred a few hours after reperfusion.

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Churchill, E. N., i D. Mochly-Rosen. "The roles of PKCδ and ϵ isoenzymes in the regulation of myocardial ischaemia/reperfusion injury". Biochemical Society Transactions 35, nr 5 (25.10.2007): 1040–42. http://dx.doi.org/10.1042/bst0351040.

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Reperfusion of ischaemic cardiac tissue is associated with increased apoptosis and oncosis, resulting in diminished heart function. Short bouts of ischaemia before the prolonged ischaemic event (ischaemic preconditioning) protect the heart from injury mediated by reperfusion. The PKC (protein kinase C) family of serine/threonine kinases are involved in many different signalling processes. Two calcium-insensitive isoforms of the novel PKC subfamily, PKCδ and ϵ, play opposing roles in ischaemia/reperfusion injury. Activation of PKCδ during reperfusion induces cell death through the regulation of mitochondrial function and induction of apoptosis and oncosis. In contrast, activation of PKCϵ before ischaemia protects mitochondrial function and diminishes apoptosis and oncosis. How can two highly homologous PKC isoenzymes play such opposing roles through the regulation of mitochondrial function? This review will highlight what is known about PKCδ and ϵ function during ischaemia/reperfusion injury and will suggest a novel regulatory pathway which determines the fate of the cell following ischaemic stress.

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Corno, Antonio, Roberto Motterlini, Laura Brenna, Francesco Santoro i Michele Samaja. "Ischaemia/reperfusion in the posthypoxaemic re-oxygenated myocardium: haemodynamic study in the isolated perfused rat heart". Perfusion 8, nr 1 (styczeń 1993): 113–18. http://dx.doi.org/10.1177/026765919300800115.

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In order to study the haemodynamics of reperfusion injury in the post hypoxaemic heart, we exposed buffer-perfused isolated rat hearts to either: (1) 20-minute low-flow ischaemia or (2) 20-minute hypoxaemia followed by re-oxygenation and further ischaemia/reperfusion. In group 2, the myocardial contractility recovered less (p <0.002) than in group 1. This model therefore represents with sufficient reliability the clinical situation where hypoxaemic hearts are re-oxgenated before ischaemia/reperfusion and receive more severe injury than hearts exposed to ischaemia/reperfusion only. To locate the major site of the injury, further data were obtained (1) with infusion of superoxide dismutase and catalase during hypoxaemia and in the first five minutes of re-oxygenation, and (2) by eliminating re-oxygenation. It appears that the major determinant of reperfusion injury in hypoxaemic hearts is to be looked for in the events underlying hypoxaemia or re-oxygenation, and is mediated by oxygen- derived free radicals.

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Grages, Anna Marei, Nicole Verhaar, Christiane Pfarrer, Gerhard Breves, Marion Burmester, Stephan Neudeck i Sabine Kästner. "Low Flow versus No Flow: Ischaemia Reperfusion Injury Following Different Experimental Models in the Equine Small Intestine". Animals 12, nr 16 (22.08.2022): 2158. http://dx.doi.org/10.3390/ani12162158.

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In experimental studies investigating strangulating intestinal lesions in horses, different ischaemia models have been used with diverging results. Therefore, the aim was to comparatively describe ischaemia reperfusion injury (IRI) in a low flow (LF) and no flow (NF) model. Under general anaesthesia, 120 min of jejunal ischaemia followed by 120 min of reperfusion was induced in 14 warmbloods. During ischaemia, blood flow was reduced by 80% (LF, n = 7) or by 100% (NF, n = 7). Intestinal blood flow and oxygen saturation were measured by Laser Doppler fluxmetry and spectrophotometry. Clinical, histological, immunohistochemical and Ussing chamber analyses were performed on intestinal samples collected hourly. Tissue oxygen saturation was significantly lower in NF ischaemia. The LF group exhibited high variability in oxygen saturation and mucosal damage. Histologically, more haemorrhage was found in the LF group at all time points. Cleaved-caspase-3 and calprotectin-stained cells increased during reperfusion in both groups. After NF ischaemia, the tissue conductance was significantly higher during reperfusion. These results aid in the selection of suitable experimental models for future studies. Although the LF model has been suggested to be more representative for clinical strangulating small intestinal disease, the NF model produced more consistent IRI.

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Li, Zy, B. Liu, J. Yu, Fw Yang, Yn Luo i Pf Ge. "Ischaemic Postconditioning Rescues Brain Injury Caused by Focal Ischaemia/Reperfusion via Attenuation of Protein Oxidization". Journal of International Medical Research 40, nr 3 (czerwiec 2012): 954–66. http://dx.doi.org/10.1177/147323001204000314.

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OBJECTIVE: To investigate the effects of ischaemic postconditioning on brain injury and protein oxidization in focal ischaemia/reperfusion. METHODS: Adult male Wistar rats ( n = 30) were randomly divided into sham-operated, ischaemia, and ischaemic postconditioning groups. Ischaemia was produced by middle cerebral artery occlusion and ischaemic postconditioning was performed using three cycles of 30-s/30-s reperfusion/reocclusion after 2 h of ischaemia. Brain infarction size, hydrogen peroxide concentration, superoxide dismutase (SOD), catalase (CAT) and proteasome activities, protein carbonyl derivatives and advanced oxidized protein products (AOPPs) were evaluated. RESULTS: The size of brain infarction after ischaemic postconditioning was significantly smaller compared with the ischaemia group, and was concomitant with significant reduction in protein carbonyl derivatives and AOPPs. The activities of SOD, CAT and proteasomes were elevated by ischaemic postconditioning compared with the ischaemia group. CONCLUSIONS: Ischaemic post-conditioning is an effective way of reducing the size and effects of brain infarction caused by focal ischaemia/reperfusion, possibly due to a decrease in oxidized protein levels. Decreasing protein oxidization may, therefore, be a useful target for preventing cerebral injury.

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BASTIAANSE, Jacqueline, Dick W. SLAAF, Mirjam G. A. oude EGBRINK, Gary L. ANDERSON, Hans VINK, Brigitte E. P. A. van der HEIJDEN i Moshe KON. "Effect of hypothermia and HTK on the microcirculation in the rat cremaster muscle after ischaemia". Clinical Science 109, nr 1 (23.06.2005): 117–23. http://dx.doi.org/10.1042/cs20040154.

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Hypothermia is an important preservation method for tissues and solid organs. The aim of the present study was to assess in rat cremaster muscle the effect of hypothermia, without or with pre-ischaemic HTK (histidine-tryptophan-ketoglutarate–Bretschneider solution) perfusion, on microvascular consequences of 4 or 6 h ischaemia and 2 h of reperfusion. Intravital microscopy was applied to examine capillary perfusion and leucocyte–endothelium interactions. The cremaster muscle was subjected to 4 or 6 h of cold (4 °C) or warm (33–34 °C) ischaemia and 2 h of reperfusion. Measurements were performed at baseline, prior to HTK perfusion and ischaemia, and at 0, 1 and 2 h after blood flow restoration. Hypothermia completely prevented the 50% reduction in capillary perfusion that was observed previously at start of reperfusion after 4 h warm ischaemia. After 6 h of warm ischaemia, perfusion resumed in only 45% of capillaries and remained at this low level during reperfusion. In contrast, only a slight decrease (<10%) in capillary perfusion was observed after 6 h of cold ischaemia. Pre-ischaemic HTK perfusion had no beneficial effect on tissue perfusion. Both hypothermia and HTK attenuated the significant increase in venular leucocyte–vessel wall interactions, which was observed after 4 h of warm ischaemia in a previous study. Combined application of both interventions had no additional effects. After 6 h of warm ischaemia, no increase in leucocyte–vessel wall interactions was observed, possibly due to venular flow reduction. In conclusion, hypothermia preserves capillary perfusion and prevents an increase in leucocyte–vessel wall interactions during reperfusion after muscle tissue ischaemia. Preischaemic perfusion of the vasculature with HTK does not improve the effects of cold storage on tissue perfusion, but attenuates the inflammatory response independently of temperature effect.

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MIZUKAMI, Yoichi, i Ken-ichi YOSHIDA. "Mitogen-activated protein kinase translocates to the nucleus during ischaemia and is activated during reperfusion". Biochemical Journal 323, nr 3 (1.05.1997): 785–90. http://dx.doi.org/10.1042/bj3230785.

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Growth factors and various cellular stresses are known to activate mitogen-activated protein (MAP) kinase, which plays a role in conveying signals from the cytosol to the nucleus. The phosphorylation of MAP kinase is thought to be a prerequisite for translocation. Here, we investigate the translocation and activation of MAP kinase during ischaemia and reperfusion in perfused rat heart. Ischaemia (0–40 min) induces the translocation of MAP kinase from the cytosol fraction to the nuclear fraction. Immunohistochemical observation shows that MAP kinase staining in the nucleus is enhanced after ischaemia for 40 min. Unexpectedly, tyrosine phosphorylation of MAP kinase is unchanged in the nuclear fraction during ischaemia, indicating that unphosphorylated MAP kinase translocates from the cytosol to the nucleus. During reperfusion (0–30 min), after ischaemia for 20 min, tyrosine phosphorylation of MAP kinase in the nuclear fraction is increased with a peak at 10 min of reperfusion. The activation is confirmed by MAP kinase activity with similar kinetics to the tyrosine phosphorylation. However, the amount of MAP kinase in the fraction is almost constant during reperfusion for 10 min. Although an upstream kinase for MAP kinase, MAP kinase/extracellular signal-regulated kinase kinase (MEK)-1, remains in the cytosol throughout ischaemia and reperfusion, MEK-2, another upstream kinase for MAP kinase, is constantly present in the nucleus as well as in the cytoplasm, based on analyses by fractionation and immunohistochemistry. Furthermore, MEK-2 activity in the nuclear fraction is rapidly increased during post-ischaemic reperfusion. These findings demonstrate that nuclear MAP kinase is activated by tyrosine phosphorylation during reperfusion, probably by MEK-2.

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Akahane, M., H. Ono, H. Ohgushi i Y. Takakura. "BONE VIABILITY OF AMPUTATED LIMBS TREATED WITH HYPOTHERMIA: ASSESSMENT BY EVALUATION OF mRNA LEVELS". Hand Surgery 10, nr 02n03 (styczeń 2005): 231–35. http://dx.doi.org/10.1142/s021881040500298x.

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We evaluated rat bone viability using a bone viability index (BVI). To evaluate hypothermic ischaemic bone injury, 21 amputated hind limbs of Fischer rats were preserved at hypothermia (4°C) for 1, 3 and 6 hours. To evaluate hypothermic ischaemia/reperfusion injury, another 28 amputated limbs were transplanted to recipient rats after hypothermic ischaemia for 3 and 6 hours, respectively. Total RNA isolated from each tibia was fractionated by electrophoresis and hybridised with 32P-labelled cDNA of GAPDH, and the radioactivity of intact and degraded GAPDH mRNA measured. BVI was calculated as follows, BVI = {A / (A + B)} × 100 , where A and B represent the radioactivities corresponding to intact and degraded GAPDH mRNA bands, respectively. In the hypothermic ischaemic insult group, BVIs were comparable to those of controls. However, in the 3-hour hypothermic ischaemia/reperfusion group, BVI was lower than that of the controls. Likewise, there was a significant difference between the 6-hour ischaemia/reperfusion group and controls. These results showed that bone viability decreased even after just a 3-hour hypothermic ischaemia/reperfusion.

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Adameova, Adriana, Slavka Carnicka, Tomas Rajtik, Adrian Szobi, Martina Nemcekova, Pavel Svec i Tana Ravingerova. "Upregulation of CaMKIIδ during ischaemia–reperfusion is associated with reperfusion-induced arrhythmias and mechanical dysfunction of the rat heart: involvement of sarcolemmal Ca2+-cycling proteins". Canadian Journal of Physiology and Pharmacology 90, nr 8 (sierpień 2012): 1127–34. http://dx.doi.org/10.1139/y2012-019.

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Although Ca2+/calmodulin-dependent protein kinase II delta (CaMKIIδ) has been implicated in development of different phenotypes of myocardial ischaemia–reperfusion injury, its involvement in arrhythmogenesis and cardiac stunning is not sufficiently elucidated. Moreover, the mechanisms by which CaMKIIδ mediates disturbances in excitation–contraction coupling, are not exactly known. To investigate this, KN-93 (0.5 µmol/L), a CaMKII inhibitor, was administered before induction of global ischaemia and reperfusion in isolated Langendorff-perfused rat hearts. Expression of CaMKIIδ and the sarcollemal Ca2+-cycling proteins, known to be activated during reperfusion, was analyzed using immunoblotting. KN-93 reduced reperfusion-induced ectopic activity and the incidence of ventricular fibrillation. Likewise, the severity of arrhythmias was lower in KN-treated hearts. During the pre-ischaemia phase, neither inotropic nor chronotropic effects were elicited by KN-93, whereas post-ischaemic contractile recovery was significantly improved. Ischaemia–reperfusion increased the expression of CaMKIIδ and sodium–calcium exchanger (NCX1) proteins without any influence on the protein content of alpha 1c, a pore-forming subunit of L-type calcium channels (LTCCs). On the other hand, inhibition of CaMKII normalized changes in the expression of CaMKIIδ and NCX1. Taken together, CaMKIIδ seems to regulate its own turnover and to be an important component of cascade integrating NCX1, rather than LTCCs that promote ischaemia–reperfusion-induced contractile dysfunction and arrhythmias.

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Liu, P. T., A. M. Symons, J. A. Howarth, P. S. Boulter i D. V. Parke. "Studies in Surgical Trauma: Oxidative Stress in Ischaemia-Reperfusion of Rat Liver". Clinical Science 86, nr 4 (1.04.1994): 453–60. http://dx.doi.org/10.1042/cs0860453.

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1. Hypovolaemic shock associated with surgical trauma has been studied in a rat liver ischaemia-reperfusion model by determination of oxidative stress, lipid peroxidation and tissue infiltration of polymorphonuclear leucocytes. 2. Liver ischaemia alone resulted in slight liver oedema and polymorphonuclear leucocyte infiltration, a slight increase in thiobarbituric acid-reacting substances (an index of lipid peroxidation) and decreases in liver reduced glutathione and total radical-trapping antioxidant parameter, indices of oxidative stress. Ischaemia plus 30 min of reperfusion further increased liver oedema, polymorphonuclear leucocyte infiltration and thiobarbituric-acid reacting substances, and further decreased liver reduced glutathione and total radical-trapping antioxidant parameter. 3. After 60 and 90 min of reperfusion, oedema (40% increase), polymorphonuclear leucocyte infiltration (40-fold increase) and thiobarbituric-acid reacting substances (20-fold increase) were maximal, and liver reduced glutathione (75–95% decrease) and total radical-trapping antioxidant parameter (85–90% decrease) were at a minimum. 4. All parameters were exacerbated by 24 h starvation. Liver reduced glutathione closely paralleled total radical-trapping antioxidant parameter, and ischaemia alone depleted both by 30% in fed rats and 50% in fasted rats. 5. Oxidative stress and lipid peroxidation were associated more with the period of reperfusion and polymorphonuclear leucocyte infiltration. Polymorphonuclear leucocyte infiltration into lung also occurred after 90 min of liver reperfusion. 6. Possible mechanisms of hepatic ischaemia-reperfusion-induced oxidative stress are discussed.

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González-Pacheco, Héctor, Aurelio Méndez-Domínguez, Salomón Hernández, Rebeca López-Marure, Maria J. Vazquez-Mellado, Cecilia Aguilar i Leticia Rocha-Zavaleta. "Pre-Conditioning with CDP-Choline Attenuates Oxidative Stress-Induced Cardiac Myocyte Death in a Hypoxia/Reperfusion Model". Scientific World Journal 2014 (2014): 1–8. http://dx.doi.org/10.1155/2014/187071.

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Background. CDP-choline is a key intermediate in the biosynthesis of phosphatidylcholine, which is an essential component of cellular membranes, and a cell signalling mediator. CDP-choline has been used for the treatment of cerebral ischaemia, showing beneficial effects. However, its potential benefit for the treatment of myocardial ischaemia has not been explored yet.Aim. In the present work, we aimed to evaluate the potential use of CDP-choline as a cardioprotector in anin vitromodel of ischaemia/reperfusion injury.Methods. Neonatal rat cardiac myocytes were isolated and subjected to hypoxia/reperfusion using the coverslip hypoxia model. To evaluate the effect of CDP-choline on oxidative stress-induced reperfusion injury, the cells were incubated with H2O2during reperfusion. The effect of CDP-choline pre- and postconditioning was evaluated using the cell viability MTT assay, and the proportion of apoptotic and necrotic cells was analyzed using the Annexin V determination by flow cytometry.Results. Pre- and postconditioning with 50 mg/mL of CDP-choline induced a significant reduction of cells undergoing apoptosis after hypoxia/reperfusion. Preconditioning with CDP-choline attenuated postreperfusion cell death induced by oxidative stress.Conclusion. CDP-choline administration reduces cell apoptosis induced by oxidative stress after hypoxia/reperfusion of cardiac myocytes. Thus, it has a potential as cardioprotector in ischaemia/reperfusion-injured cardiomyocytes.

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SARIS, N. E. L., i K. O. ERIKSSON. "Mitochondrial dysfunction in ischaemia-reperfusion". Acta Anaesthesiologica Scandinavica 39 (wrzesień 1995): 171–76. http://dx.doi.org/10.1111/j.1399-6576.1995.tb04353.x.

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Fuller, Barry J. "Ischaemia/Reperfusion Injury and inflammation". Transplantation 69, nr 3 (luty 2000): 327–30. http://dx.doi.org/10.1097/00007890-200002150-00002.

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Eltzschig, Holger K., i Charles D. Collard. "Vascular ischaemia and reperfusion injury". British Medical Bulletin 70, nr 1 (1.01.2004): 71–86. http://dx.doi.org/10.1093/bmb/ldh025.

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Tan, P. "Book Review: Ischaemia-reperfusion Injury". European Journal of Vascular and Endovascular Surgery 18, nr 6 (grudzień 1999): 546–47. http://dx.doi.org/10.1053/ejvs.1999.0896.

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Wu, Li-Ning, Rui Hu i Jun-Ma Yu. "Morphine and myocardial ischaemia-reperfusion". European Journal of Pharmacology 891 (styczeń 2021): 173683. http://dx.doi.org/10.1016/j.ejphar.2020.173683.

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Ch'en, F. F. T., R. D. Vaughan-Jones, K. Clarke i D. Noble. "Modelling myocardial ischaemia and reperfusion". Progress in Biophysics and Molecular Biology 69, nr 2-3 (marzec 1998): 515–38. http://dx.doi.org/10.1016/s0079-6107(98)00023-6.

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Carden, Donna L., i D. Neil Granger. "Pathophysiology of ischaemia-reperfusion injury". Journal of Pathology 190, nr 3 (luty 2000): 255–66. http://dx.doi.org/10.1002/(sici)1096-9896(200002)190:3<255::aid-path526>3.0.co;2-6.

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Ferrari, Roberto. "Myocardial metabolism during ischaemia-reperfusion". Journal of Molecular and Cellular Cardiology 24 (maj 1992): 32. http://dx.doi.org/10.1016/0022-2828(92)90125-j.

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Busuttil, R. "Liver ischaemia and reperfusion injury". British Journal of Surgery 94, nr 7 (2007): 787–88. http://dx.doi.org/10.1002/bjs.5921.

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Defraigne, J. O., J. Pincemail, C. Franssen, M. Meurisse, T. Defechereux, C. Philippart, D. Serteyn, M. Lamy, C. Deby i R. Limet. "In Vivo free Radical Production after Cross-Clamping and Reperfusion of the Renal Artery in the Rabbit". Cardiovascular Surgery 1, nr 4 (sierpień 1993): 343–49. http://dx.doi.org/10.1177/096721099300100406.

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Postischaemic reperfusion injury is often attributed to the generation of oxygenated free radicals which may subsequently promote lipid peroxidation in cell membranes. Electron paramagnetic resonance spectroscopy in association with the spin trap molecule α-phenyl- N-tert-butyl-nitrone allowed direct confirmation of lipid free radical production after renal ischaemia-reperfusion in an in vivo rabbit model. A 60-min period of ischaemia followed by reperfusion caused free radical production twofold greater than after 15min of ischaemia. Glutathione and a-tocopherol have been measured in renal tissue, as indirect markers of lipid peroxidation. After 15min of ischaemia followed by 10min of reperfusion, the mean(s.e.m.) glutathione content of the ischaemic kidney was slightly but significantly reduced by 11.9(2.5)% ( P < 0.003). The content of α-tocopherol was unchanged. However, 10min of reperfusion following 60 min of ischaemia led to significant decrease in mean(s.e.m.) content of both glutathione (30.4(3.7)%) (2.23(0.2) versus 3.14(0.18) μmol/g wet tissue, ( P < 0.001) and α-tocopherol (46.1(7.8)%) (0.57(0.10) versus 1.09(0.14) μg/g wet tissue. P < 0.001) when compared to the control kidney. Under these experimental conditions, desferrioxamine (15mg/kg administered intravenously before inducing ischaemia), a drug known to limit free radical production, significantly limited the decrease of α-tocopherol to 20.8(6.4)% (0.83(0.08) versus 1.05(0.04) μg/g wet tissue. P < 0.05), but did not prevent glutathione consumption in the reperfused kidney.

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Tang, LL, K. Ye, XF Yang i JS Zheng. "Apocynin Attenuates Cerebral Infarction after Transient Focal Ischaemia in Rats". Journal of International Medical Research 35, nr 4 (lipiec 2007): 517–22. http://dx.doi.org/10.1177/147323000703500411.

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This study investigated whether inhibition of reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase attenuates cerebral infarction after transient focal ischaemia in rats. Focal ischaemia (1.5 h) was produced in male Sprague-Dawley rats (250 − 280 g) by middle cerebral artery occlusion. Some rats also received treatment with 50 mg/kg apocynin, a NADPH oxidase inhibitor, by intraperitoneal injection 30 min prior to reperfusion. Two hours after reperfusion, brains were harvested to measure NADPH oxidase activity and superoxide levels. After 24 h, the remaining brains were harvested to investigate infarct size. NADPH oxidase activity and superoxide level were all augmented 2 h after reperfusion compared with controls. Apocynin treatment significantly reduced NADPH oxidase activity and superoxide levels. Cerebral infarct size was significantly smaller in the apocynin-treated group compared with those undergoing ischaemia/reperfusion alone. These results indicate that inhibition of NADPH oxidase attenuates cerebral infarction after transient focal ischaemia in rats, suggesting that inhibition of NADPH oxidase may provide a therapeutic strategy for ischaemic stroke.

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Vaughan, D. L., Y. A. B. D. Wickramasinghe, G. I. Russell, M. S. Thorniley, R. F. Houston, E. Ruban i P. Rolfe. "Is Allopurinol Beneficial in the Prevention of Renal Ischaemia—Reperfusion Injury in the Rat?: Evaluation by Near-Infrared Spectroscopy". Clinical Science 88, nr 3 (1.03.1995): 359–64. http://dx.doi.org/10.1042/cs0880359.

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1. The role of allopurinol in the protection of kidney function following ischaemia—reperfusion injury has been investigated using the novel technique of near-infrared spectroscopy. 2. An in vivo model of rat kidney ischaemia was used, with the expected falls in blood and tissue oxygenation seen and confirmed by near-infrared spectroscopy. 3. Allopurinol infusion increased the rate of reperfusion of oxygenated blood seen in control rats (P < 0.05). 4. Allopurinol enhanced the rate of tissue oxygenation during early reperfusion (P < 0.01). 5. This study provides further evidence for the proposed benefits of allopurinol in ischaemia—reperfusion injury. Furthermore, the potential of near-infrared spectroscopy as a technique of value in interventional studies of this nature is confirmed.

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Xiao, Lili, Yulei Gu, Gaofei Ren, Linlin Chen, Liming Liu, Xiaofang Wang i Lu Gao. "miRNA-146a Mimic Inhibits NOX4/P38 Signalling to Ameliorate Mouse Myocardial Ischaemia Reperfusion (I/R) Injury". Oxidative Medicine and Cellular Longevity 2021 (27.07.2021): 1–10. http://dx.doi.org/10.1155/2021/6366254.

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Evidence suggests that miR-146a is implicated in the pathogenesis of cardiovascular diseases; however, the role of miR-146a in myocardial ischaemia reperfusion (I/R) injury is unclear. The aim of this study was to explore the functional role of miR-146a in myocardial ischaemia reperfusion injury and the underlying mechanism. C57BL/6J mice were subjected to 45 min of ischaemia and 1 week of reperfusion to establish a myocardial I/R injury model. A miR-146a mimic (0.5 mg/kg) was administered intravenously at the beginning of the ischaemia process. Neonatal rat cardiomyocytes were also subjected to hypoxia/reperfusion (H/R). Cells were treated with the miR-146a mimic or antagonist. As a result, the miR-146a mimic attenuated H/R-induced cardiomyocyte injury, as evidenced by increased cell viability and reduced lactate dehydrogenase (LDH) levels. In addition, the miR-146a mimic inhibited oxidative stress in cells suffering from H/R injury. Moreover, the miR-146a antagonist exerted adverse effects in vitro. In mice with myocardial I/R injury, the miR-146a mimic preserved cardiac function and reduced the infarction area and fibrosis. Moreover, the miR-146a mimic decreased the inflammatory response and reactive oxygen species (ROS) accumulation in mouse hearts. Mechanistically, we found that miR-146a directly regulated the transcription of NOX4, which subsequently affected P38 signalling in cardiomyocytes. When we knocked down NOX4, the effects of the miR-146a antagonist in worsening the cell condition were counteracted in in vitro experiments. Taken together, the results suggest that miR-146a protects against myocardial ischaemia reperfusion injury by inhibiting NOX4 signalling. The miR-146a mimic may become a potential therapeutic approach for patients with myocardial ischaemia reperfusion.

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