Journal articles on the topic 'Ischaemia'
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1
Li, Zy, B. Liu, J. Yu, Fw Yang, Yn Luo, and Pf Ge. "Ischaemic Postconditioning Rescues Brain Injury Caused by Focal Ischaemia/Reperfusion via Attenuation of Protein Oxidization." Journal of International Medical Research 40, no. 3 (June 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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Nunn, J. A., J. A. Gray, and H. Hodges. "Neurotoxic Dorsal CA1 Lesions versus 4 VO Ischaemic Lesions: Behavioural Comparisons." Behavioural Neurology 11, no. 4 (1999): 217–26. http://dx.doi.org/10.1155/1999/603123.
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Anterograde amnesia, a common consequence of transient cerebral ischaemia, has been attributed to cell loss in the hippocampal CA1 subfield. However, variable, widespread damage outside hippocampal CA1 can also occur following ischaemia. We compared the functional consequences of ischaemia and ibotenate acid CA1 lesions on 2 spatial memory tasks (water maze ‘place’ and ‘matching-to-position’) to address the possibility that extra-CA1 loss contributes to ischaemia-induced memory deficits in the rat. During place task acquisition, ischaemic rats showed deficits on more measures than ibotenic rats, and during a 1 min probe trial, only ischaemic rats were impaired. On the matching-to-position task, ibotenic rats showed greater impairment than ischaemic rats in terms of one-trial learning, whereas ischaemic rats were more impaired after Trial 2. Ischaemia and ibotenic acid lesions resulted in equivalent CA1 loss, but silver impregnation revealed additional extra-CA1 cell loss in ischaemic rats. Together with the greater behavioural deficits of ischaemic rats, these data indicate a role for extra-CA1 cell loss in ischaemia-induced memory impairments in both animals and humans.
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Saeid, Feyzizadeh, Javadi Aniseh, Badalzadeh Reza, and Vafaee S. Manouchehr. "Signaling mediators modulated by cardioprotective interventions in healthy and diabetic myocardium with ischaemia–reperfusion injury." European Journal of Preventive Cardiology 25, no. 14 (February 14, 2018): 1463–81. http://dx.doi.org/10.1177/2047487318756420.
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Ischaemic heart diseases are one of the major causes of death in the world. In most patients, ischaemic heart disease is coincident with other risk factors such as diabetes. Patients with diabetes are more prone to cardiac ischaemic dysfunctions including ischaemia–reperfusion injury. Ischaemic preconditioning, postconditioning and remote conditionings are reliable interventions to protect the myocardium against ischaemia–reperfusion injuries through activating various signaling pathways and intracellular mediators. Diabetes can disrupt the intracellular signaling cascades involved in these myocardial protections, and studies have revealed that cardioprotective effects of the conditioning interventions are diminished in the diabetic condition. The complex pathophysiology and poor prognosis of ischaemic heart disease among people with diabetes necessitate the investigation of the interaction of diabetes with ischaemia–reperfusion injury and cardioprotective mechanisms. Reducing the outcomes of ischaemia–reperfusion injury using targeted strategies would be particularly helpful in this population. In this study, we review the protective interventional signaling pathways and mediators which are activated by ischaemic conditioning strategies in healthy and diabetic myocardium with ischaemia–reperfusion injury.
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Dart, A. M., and R. A. Riemersma. "Origins of endogenous noradrenaline overflow during reperfusion of the ischaemic rat heart." Clinical Science 74, no. 3 (March 1, 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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Schwarting, Sönke, and Harald Neumann. "Immunoregulatory Neuroprotection of Cerebral Ischaemia by Haematopoietic Stem and Precursor Cells." European Neurological Review 4, no. 2 (2009): 42. http://dx.doi.org/10.17925/enr.2009.04.02.42.
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Cerebral ischaemia leads to early immune system activation followed by delayed immunosuppression. Post-ischaemic inflammation contributes to neurodegeneration. Although experimental approaches using adult stem or precursor cells have repeatedly demonstrated neuroprotective effects in cerebral ischaemia, the underlying mechanism of cell-mediated neuroprotection is still debated. It was suggested that stem or precursor cells invade ischaemic brain regions and act locally. However, recent data demonstrate that systemically transplanted stem or precursor cells have strong immunoregulatory effects leading to reduced post-ischaemic brain tissue inflammation. This article argues that the systemic balance of the immune system might explain the reduced neurodegeneration observed after stem cell treatment in cerebral ischaemia. Consequently, systemic immunoregulatory neuroprotection using stem and precursor cells should be considered an important therapeutic option to prevent post-ischaemic neurodegeneration in cerebral ischaemia.
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Park, C. K., D. G. Nehls, D. I. Graham, G. M. Teasdale, and J. McCulloch. "Focal Cerebral Ischaemia in the Cat: Treatment with the Glutamate Antagonist MK-801 after Induction of Ischaemia." Journal of Cerebral Blood Flow & Metabolism 8, no. 5 (October 1988): 757–62. http://dx.doi.org/10.1038/jcbfm.1988.124.
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The effects of the glutamate N-methyl-D-aspartate receptor antagonist MK-801 in reducing ischaemic brain damage have been examined in anaesthetised cats, with drug treatment being initiated 2 h after the induction of cerebral ischaemia. Focal cerebral ischaemia was produced by permanent occlusion of one middle cerebral artery, and the animals were killed 6 h later. The amount of early irreversible ischaemic damage was assessed at 16 predetermined stereotactic planes. Treatment with MK-801 (5 mg/kg, i.v.) 2 h after middle cerebral artery occlusion reduced significantly the volume of ischaemic damage (from 1,625 ± 384 mm3 of the cerebral hemisphere in vehicle-treated cats to 792 ± 385 mm3 in MK-801-treated cats). The demonstration of reduced ischaemic brain damage with MK-801, when the agent is administered after the induction of ischaemia, extends the therapeutic potential of such agents in the treatment of focal cerebral ischaemia in humans.
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Churchill, E. N., and D. Mochly-Rosen. "The roles of PKCδ and ϵ isoenzymes in the regulation of myocardial ischaemia/reperfusion injury." Biochemical Society Transactions 35, no. 5 (October 25, 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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AL-QATTAN, M. M. "Ischaemia-Reperfusion Injury." Journal of Hand Surgery 23, no. 5 (October 1998): 570–73. http://dx.doi.org/10.1016/s0266-7681(98)80003-x.
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Prolonged ischaemia sometimes occurs in replantation and free flap surgery. The re-establishment of circulatory flow to the ischaemic tissue leads to a cascade of events which augments tissue necrosis. This paper reviews the pathophysiology of this ischaemia-reperfusion injury and discusses different methods to modulate this injury.
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Simon, R., and Z. Xiong. "Acidotoxicity in brain ischaemia." Biochemical Society Transactions 34, no. 6 (October 25, 2006): 1356–61. http://dx.doi.org/10.1042/bst0341356.
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Intracellular calcium toxicity remains the central feature in the pathophysiology of ischaemic cell death in brain. Glutamate-gated channels have been thought to be the major sites of ischaemia-induced toxic calcium entry, but the failure of glutamate antagonists in clinical trials has suggested that glutamate-independent mechanisms of calcium entry during ischaemia must exist and may prove central to ischaemic injury. We have shown that ASICs (acid-sensing ion channels) in brain are glutamate-independent vehicles of calcium flux and transport calcium in greater measure in the setting of the two major neurochemical components of ischaemia: acidosis and substrate depletion. Pharmacological blockade of ASICs markedly attenuates stroke injury with a robust therapeutic time window of 5 h following stroke onset. Here, we describe this new mechanism of calcium toxicity in brain ischaemia and offer a potential new therapy for stroke.
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HILLIER, C., R. D. SAYERS, P. A. C. WATT, R. NAYLOR, P. R. F. BELL, and H. THURSTON. "Altered small artery morphology and reactivity in critical limb ischaemia." Clinical Science 96, no. 2 (February 1, 1999): 155–63. http://dx.doi.org/10.1042/cs0960155.
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Although the pathophysiology of critical limb ischaemia is poorly understood, there is evidence that the condition of the small arteries may determine the outcome of revascularization procedures. This study was designed to investigate the effects of critical limb ischaemia on the structure and function of the small arteries in the leg. Small arteries (< 500 μm) from proximal (non-ischaemic) and distal (ischaemic) sites were obtained from patients undergoing bypass surgery for critical limb ischaemia and mounted in a myograph. Reactivity and morphological measurements were carried out and compared with controls. Control vessels from the thigh and calf showed no difference in media to lumen ratio. However, a comparison of ischaemic and non-ischaemic vessels from the patients with critical limb ischaemia showed significant thinning of the ischaemic vessel wall. Contraction studies using noradrenaline and angiotensin II revealed a significant decrease in the response of ischaemic vessels compared with the non-ischaemic vessels from the same patient. Moreover, these differences in reactivity were still apparent after the responses were corrected for wall thickness. Endothelial function assessed using the endothelium-dependent agonists acetylcholine and bradykinin showed a significantly impaired relaxation response to acetylcholine but not to bradykinin in the ischaemic vessels, and acetylcholine-induced relaxation was not improved after incubation with indomethacin. There was no change in the response to the endothelium-independent cAMP-mediated vasodilator iloprost but a significant impairment to sodium nitroprusside which acts via cGMP. These results suggest that small arteries in critical limb ischaemia are altered in both structure and function, with vessel wall thinning and impaired responses to acetylcholine and sodium nitroprusside.
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Dimitrijevic, I., M. Micev, Dj Saranovic, V. Markovic, J. Petrovic, S. Antic, A. Sekulic, and Z. Krivokapic. "Ischaemic colitis - review." Acta chirurgica Iugoslavica 55, no. 3 (2008): 89–95. http://dx.doi.org/10.2298/aci0803089d.
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Colonic ischaemia, commonly referred to as ischaemic colitis, is the most common type of intestinal ischaemia. The term "ischaemic colitis" was used by Marston (1966) with three typical patterns of injury described: transient reversible ischaemia, ischaemic ulcers with stricturing, and gangrenous ischaemic colitis. Dominant presenting symptoms were colicky abdominal pain, vomiting, bloody diarrhea, and hematochezia. Patients often have minimal signs on clinical examination. Most patients were diagnosed at colonoscopy. Two regions that are believed to be anatomically vulnerable to ischemic disease are "Griffith?s point", at the splenic flexure and "Sudeck?s critical point", of the Drummond marginal artery. Clinically, ischaemic colitis is classified as non-gangrenous or gangrenous. Non-gangrenous ischaemic colitis involves the mucosa and submucosa and accounts for 80-85 percent of all cases of ischaemic colitis. Non-gangrenous ischaemic colitis is further subclassified into transient, reversible ischaemic colitis with a less severe form of injury and chronic, non-reversible ischaemic colitis, which includes chronic colitis and stricture and has a more severe form of injury. Gangrenous ischaemic colitis accounts for the remaining 15-20 percent of cases and manifests as the most severe form of injury. It includes acute fulminant ischaemia with transmural infarction that may progress to necrosis and death. Specific indications for operation include peritonitis, perforation, recurrent fever or sepsis, clinical deterioration in patients refractory to medical management. Relative indications include fulminant colitis, massive hemorrhage, chronic protein losing colopathy, and symptomatic ischemic structure.
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Szijártó, Attila. "Az ischaemiatolerancia növelésének lehetőségei a májsebészetbenr." Magyar Sebészet 61, no. 3 (June 1, 2008): 128–35. http://dx.doi.org/10.1556/maseb.61.2008.3.5.
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Absztrakt A szerző az ischaemia-reperfusio kapcsán fellépő kórállapotokat elemzi kísérletes májműtétek kapcsán. Célkitűzés: Kísérleteim célja a máj kiterjesztett, műtéti resectiója során fellépő ischaemia és az ischaemiatolerancia, továbbá egy, endogén defenzív mechanizmussal bíró ischaemiás preconditionálás (IP), illetve az oxidatív stressz hatására aktiválódó poli(ADP-ribóz) polimeráz enzimet gátló vegyület (PJ-34) és az antioxidáns potenciállal bíró glutamin (Gln) kísérletes vizsgálata volt IR modellben. Anyagok és módszer: Az első kísérletben Wistar-patkányok máján változó időtartamú (30-45-60-90 perc) segmentalis ischaemiát hoztunk létre, IP-sal kiegészítve. A második kísérletsorozatban PJ-34-, Gln-előkezelés történt 60 perces ischaemiával. A microcirculatiós változásokat laser Doppler flowmeterrel mértük. A módszer alkalmazásához új technikai kritériumokat állítottunk fel, illetve a kapott értékeket, matematikai analízist követően, statisztikai feldolgozásra alkalmassá tettük. Vizsgáltuk a szövettani változásokat, az antioxidáns-szinteket, konvencionális laboratóriumi és TNF-α szinteket mértünk. Eredmények, megbeszélés: A máj a 30 perces ischaemiát jól tolerálja, a 45 és 60 perces kirekesztés jelentős áramlásbeli változásokat okoz. A 90 perces ischaemia nem tolerálható. Az IP szignifikáns reperfusiós áramlási javulást és szérum-TNF-α csökkenést okoz a 45 és 60 perces ischaemia előtt alkalmazva. PJ-34 PARP-inhibitor-, illetve Gln-előkezelés, 60 perc reperfusiót vizsgálva, javítja a microcirculatiót. Aktivált kaszpáz-3 immunhisztokémiával végzett vizsgálatok során a PJ-34 PARP-inhibitor- és Gln-előkezelések hatására szignifikánsan magasabb apoptosis volt detektálható a kontrollcsoporthoz képest. A májszöveti és szérumantioxidáns-paramétereket mind az IP, mind a Gln-előkezelés javították.
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Farkasinszky, Gergely, Judit Szabó Péliné, Péter Károlyi, Szilvia Rácz, Noémi Dénes, Tamás Papp, József Király, et al. "In Vivo Imaging of Acute Hindlimb Ischaemia in Rat Model: A Pre-Clinical PET Study." Pharmaceutics 16, no. 4 (April 15, 2024): 542. http://dx.doi.org/10.3390/pharmaceutics16040542.
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Background: To better understand ischaemia-related molecular alterations, temporal changes in angiogenic Aminopeptidase N (APN/CD13) expression and glucose metabolism were assessed with PET using a rat model of peripheral arterial disease (PAD). Methods: The mechanical occlusion of the base of the left hindlimb triggered using a tourniquet was applied to establish the ischaemia/reperfusion injury model in Fischer-344 rats. 2-[18F]FDG and [68Ga]Ga-NOTA-c(NGR) PET imaging performed 1, 3, 5, 7, and 10 days post-ischaemia induction was followed by Western blotting and immunohistochemical staining for APN/CD13 in ischaemic and control muscle tissue extracts. Results: Due to a cellular adaptation to hypoxia, a gradual increase in [68Ga]Ga-NOTA-c(NGR) and 2-[18F]FDG uptake was observed from post-intervention day 1 to 7 in the ischaemic hindlimbs, which was followed by a drop on day 10. Conforming pronounced angiogenic recovery, the NGR accretion of the ischaemic extremities differed significantly from the controls 5, 7, and 10 days after ischaemia induction (p ≤ 0.05), which correlated with the Western blot and immunohistochemical results. No remarkable radioactivity was depicted between the normally perfused hindlimbs of either the ischaemic or the control groups. Conclusions: The PET-based longitudinal assessment of angiogenesis-associated APN/CD13 expression and glucose metabolism during ischaemia may continue to broaden our knowledge on the pathophysiology of PAD.
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Nedvig, Klára, Edina Völgyi, György Wéber, Erzsébet Rőth, and Andrea Ferencz. "Az ischaemiás posztkondicionálás hatása az oxidatív stresszre és a szöveti struktúrára vékonybél meleg ischaemiás és autotranszplantációs modellekben." Magyar Sebészet 64, no. 6 (December 1, 2011): 294–300. http://dx.doi.org/10.1556/maseb.64.2011.6.5.
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Absztrakt Bevezetés/célkitűzés: Az ischaemiás posztkondicionálás (IPO) hatását kívántuk vizsgálni vékonybél meleg ischaemia/reperfusiós (I/R) és hideg konzerválást követő autotranszplantációs modellekben. Anyag és módszerek: Sertéseken (Σn = 32, n = 2/csoport) az arteria mesenterica superior leszorításával meleg ischaemiát hoztunk létre 1, 3 és 6 órán át. A 3 órás reperfusiót megelőzően 3 ciklusban IPO-t végeztünk ciklusonként 30 másodperc ischaemia és 30 másodperc reperfusio alkalmazásával. A hideg ischaemiás csoportokban a vékonybelet University of Wisconsin oldatban konzerváltuk 1, 3 és 6 órán keresztül. A 3 órás reperfusio előtt a fenti IPO protokollt alkalmaztuk. Bélmintákat vettünk a laparotomiát követően (kontroll) és a reperfusio végén. Az oxidatívstressz-markerek közül meghatároztuk a szöveti malondialdehid (MDA) és redukált glutation (GSH) koncentrációját, illetve a szuperoxid-dizmutáz (SOD) aktivitását. A szöveti károsodást Park-féle klasszifikáció és Scion Image Software kvantitatív kiértékeléssel határoztuk meg. Eredmények: Az oxidatívstressz-paraméterek közül az IPO szignifikánsan csökkentette a reperfusio végi lipidperoxidációt, és az endogén antioxidánsok (GSH, SOD) védő szerepe szignifikáns mértékben megőrződött. A szöveti károsodás a meleg ischaemia és a konzerválás idejének emelkedésével szignifikánsan nőtt. Az IPO minden csoportban szignifikánsan csökkentette a bélfal károsodását (p < 0,05). Következtetések: A meleg I/R és hideg konzerválást követő autotranszplantációs modellekben az IPO szignifikánsan csökkentette mind az oxidatív stressz, mind a szövetkárosodások mértékét.
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Akahane, M., H. Ono, H. Ohgushi, and Y. Takakura. "BONE VIABILITY OF AMPUTATED LIMBS TREATED WITH HYPOTHERMIA: ASSESSMENT BY EVALUATION OF mRNA LEVELS." Hand Surgery 10, no. 02n03 (January 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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Di Marco, Stefano, Beatrice Boldrini, Umberto Conti, Gabriella Marcucci, Cecilia Morgantini, Ele Ferrannini, and Andrea Natali. "Effects of GIK (glucose–insulin–potassium) on stress-induced myocardial ischaemia." Clinical Science 119, no. 1 (April 7, 2010): 37–44. http://dx.doi.org/10.1042/cs20090438.
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Despite the evidence in experimental animal models that insulin, or GIK (glucose–insulin–potassium), improves left ventricular function and perfusion during both acute and chronic ischaemia, clinical studies have generated conflicting results. We tested the hypothesis that pretreatment with GIK attenuates the vascular and functional effects of stress-induced myocardial ischaemia in humans. Twenty-two patients with evidence of inducible myocardial ischaemia were enrolled; 11 patients with normal ventricular function underwent two dipyridamole echocardiography tests, and 11 with regional contractility defects from previous myocardial infarction were submitted to two ECG exercise tests combined with 201Tl myocardial perfusion scintigraphy; the tests were preceded by 60 min of either normal saline or an isoglycaemic GIK infusion. On a stress echocardiogram, a 30% reduction in the severity of ischaemia was observed. On ECG ergometry, GIK infusion slightly increased the time to ischaemia (+0.6 min, P=0.07); however, the higher workload (+8%, P=0.07) was achieved at a similar rate–pressure plateau. On scintigraphy, an increase in ischaemic segments (+48%, P<0.001) was imaged mainly at the expense of viable (but non-ischaemic) and non-viable segments, which were reduced by 60%. GIK affected stress-induced left ventricular underperfusion only marginally (GIK: 39.7±2.5 compared with saline: 35.4±2.2 units, P<0.05), but significantly improved its acute reversibility (−42±4 compared with −25±4%, P<0.001). We conclude that GIK pretreatment attenuates the effect of ischaemia on myocardial contractility, slightly improves exercise tolerance and causes a more rapid and diffuse recovery of post-ischaemic reperfusion.
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Martins-Marques, Tania, Steve Catarino, Monica Zuzarte, Carla Marques, Paulo Matafome, Paulo Pereira, and Henrique Girão. "Ischaemia-induced autophagy leads to degradation of gap junction protein connexin43 in cardiomyocytes." Biochemical Journal 467, no. 2 (April 2, 2015): 231–45. http://dx.doi.org/10.1042/bj20141370.
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GJIC (gap junction intercellular communication) between cardiomyocytes is essential for synchronous heart contraction and relies on Cx (connexin)-containing channels. Increased breakdown of Cx43 has been often associated with various cardiac diseases. However, the mechanisms whereby Cx43 is degraded in ischaemic heart remain unknown. The results obtained in the present study, using both HL-1 cells and organotypic heart cultures, show that simulated ischaemia induces degradation of Cx43 that can be prevented by chemical or genetic inhibitors of autophagy. Additionally, ischaemia-induced degradation of Cx43 results in GJIC impairment in HL-1 cells, which can be restored by autophagy inhibition. In cardiomyocytes, ubiquitin signals Cx43 for autophagic degradation, through the recruitment of the ubiquitin-binding proteins Eps15 (epidermal growth factor receptor substrate 15) and p62, that assist in Cx43 internalization and targeting to autophagic vesicles, via LC3 (light chain 3). Moreover, we establish that degradation of Cx43 in ischaemia or I/R (ischaemia/reperfusion) relies upon different molecular players. Indeed, degradation of Cx43 during early periods of ischaemia depends on AMPK (AMP-activated protein kinase), whereas in late periods of ischaemia and I/R Beclin 1 is required. In the Langendorff-perfused heart, Cx43 is dephosphorylated in ischaemia and degraded during I/R, where Cx43 degradation correlates with autophagy activation. In summary, the results of the present study provide new evidence regarding the molecular mechanisms whereby Cx43 is degraded in ischaemia, which may contribute to the development of new strategies that aim to preserve GJIC and cardiac function in ischaemic heart.
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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, and Moshe KON. "Effect of hypothermia and HTK on the microcirculation in the rat cremaster muscle after ischaemia." Clinical Science 109, no. 1 (June 23, 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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Klotzsche - von Ameln, Anne, Sebastian Cremer, Jedrzej Hoffmann, Peggy Schuster, Sherif Khedr, Irina Korovina, Maria Troullinaki, et al. "Endogenous developmental endothelial locus-1 limits ischaemia- related angiogenesis by blocking inflammation." Thrombosis and Haemostasis 117, no. 06 (2017): 1150–63. http://dx.doi.org/10.1160/th16-05-0354.
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SummaryWe have recently identified endothelial cell-secreted developmental endothelial locus-1 (Del-1) as an endogenous inhibitor of β2-integrin–dependent leukocyte infiltration. Del-1 was previously also implicated in angiogenesis. Here, we addressed the role of endogenously produced Del-1 in ischaemia-related angiogenesis. Intriguingly, Del-1–deficient mice displayed increased neovascularisation in two independent ischaemic models (retinopathy of prematurity and hind-limb ischaemia), as compared to Del-1–proficient mice. On the contrary, angiogenic sprouting in vitro or ex vivo (aortic ring assay) and physiological developmental retina angiogenesis were not affected by Del-1 deficiency. Mechanistically, the enhanced ischaemic neovascularisation in Del-1-deficiency was linked to higher infiltration of the ischaemic tissue by CD45+ haematopoietic and immune cells. Moreover, Del-1-deficiency promoted β2-integrin–dependent adhesion of haematopoietic cells to endothelial cells in vitro, and the homing of hematopoietic progenitor cells and of immune cell populations to ischaemic muscles in vivo. Consistently, the increased hind limb ischaemia-related angiogenesis in Del-1 deficiency was completely reversed in mice lacking both Del-1 and the β2-integrin LFA-1. Additionally, enhanced retinopathy-associated neovascularisation in Del-1-deficient mice was reversed by LFA-1 blockade. Our data reveal a hitherto unrecognised function of endogenous Del-1 as a local inhibitor of ischaemia-induced angiogenesis by restraining LFA-1–dependent homing of pro-angiogenic haematopoietic cells to ischaemic tissues. Our findings are relevant for the optimisation of therapeutic approaches in the context of ischaemic diseases.Supplementary Material to this article is available online at www.thrombosis-online.com.
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Cheng, SF, A. Zarkali, T. Richards, R. Simister, and A. Chandratheva. "Carotid artery stenosis, an underestimated cause of stroke recurrence in patients with ischaemic monocular visual loss." Annals of The Royal College of Surgeons of England 101, no. 8 (November 2019): 579–83. http://dx.doi.org/10.1308/rcsann.2019.0071.
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Introduction Isolated monocular ischaemic events are thought to be low risk for stroke recurrence. In the presence of carotid stenosis however, the risks should not be treated similarly and surgical intervention should be considered at an early stage. The aim of this study was to determine the vascular risk profile and stroke recurrence in patients with ischaemic monocular visual loss. Methods and methods Consecutive records for all patients with monocular ischaemia were reviewed from January 2014 to October 2016. Stroke, transient ischaemic attack or monocular ischaemia recurrence within 90 days were recorded. Carotid stenosis was assessed with duplex ultrasound, computed tomography or magnetic resonance angiography. Results In total, 400 patients presented with monocular ischaemia; 391 had carotid imaging (97.8%). Causality was symptomatic carotid stenosis ≥ 50% in 53 (13.6%), including carotid stenosis ≥ 70% in 31 (7.9%). Patients with permanent visual loss (n = 131) were more likely to have significant stenosis compared with patients with transient visual loss (n = 260), 19.8% compared with 10.4% (P = 0.012). Recurrent stroke, transient ischaemic attack or monocular ischaemia within 90 days after presentation occurred in three patients (5.7%) in the carotid stenosis group, compared to three (0.9%) who did not have stenosis (P = 0.035). Age, male sex and hypertension were associated with carotid stenosis but hypercholesterolaemia, diabetes and smoking were not. Conclusions Carotid stenosis ≥ 50% is present in patients with ocular ischaemia in approximately 20% of those with persistent visual loss and in 10% with transient visual loss. Those with carotid stenosis have a higher risk of stroke recurrence and should be considered urgent surgical intervention as other forms of stroke.
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Knight, Kenneth R., Michael F. Angel, Diana A. Lepore, Paul A. Abbey, Laurence I. Arnold, Kathleen A. Gray, Cary G. Mellow, and Bernard McC O'Brien. "Secondary Ischaemia in Rabbit Skin Flaps: The Roles Played by Thromboxane and Free Radicals." Clinical Science 80, no. 3 (March 1, 1991): 235–40. http://dx.doi.org/10.1042/cs0800235.
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1. Biochemical mechanisms of ischaemia were investigated in rabbit skin flaps subjected to 2 h of primary ischaemia then, 24 h later, to 4 h of secondary ischaemia. During secondary ischaemia, flaps underwent either total ischaemia (arterial and venous blood supply occluded) or partial ischaemia (vein only occluded). Some of these flaps were treated at the time of reperfusion with the free-radical scavenger superoxide dismutase (EC 1.15.1.1) and/or the thromboxane synthetase inhibitor UK-38,485. 2. After 30 min of reperfusion, superoxide dismutase treatment significantly reduced blood thromboxane levels, elevated during ischaemia. Superoxide dismutase also reduced tissue levels of malonyldialdehyde and xanthine oxidase, indicators of free-radical damage, and restored the depleted tissue levels of superoxide dismutase. 3. UK-38,485 treatment failed to significantly alter any of these tissue free-radical parameters, although this agent significantly reduced blood thromboxane levels. 4. Combined superoxide dismutase plus UK-38,485 treatment was not significantly better than either treatment alone with respect to any parameter. 5. Partial ischaemia led to consistently higher levels of tissue free radicals and blood thromboxane than did total ischaemia. Thus partial ischaemia appears to result in greater free-radical damage than total ischaemia. 6. These results are consistent with the hypothesis that thromboxane acts as a mediator for free-radical damage in the ischaemic changes within the flap.
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Duggie, Alastair, and Jacob McDermott. "Anaesthetic preconditioning and its role in protecting patients at risk of myocardial ischaemia." Journal of Global Medicine 1, no. 2 (December 31, 2021): e45. http://dx.doi.org/10.51496/jogm.v1.45.
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Ischaemic preconditioning is a phenomenon where prior minor ischaemic events allows organs to better withstand further episodes of ischaemia. Preconditioning downgrades the effects of ischaemia from necrosis to apoptosis to cell survival. It occurs in a wide variety of tissues, but it is most widely studied in the heart, and it occurs after a range of stimuli including hypoxia and the use of volatile anaesthetic agents. In this article, we look at the basic science, mechanisms, and potential uses of preconditioning.
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Ferwana, O. S., S. C. Pirie, and D. J. Potts. "Effect of Phosphate-Buffered Sucrose Flush Solution upon the Initial Phase of Ischaemic Acute Renal Failure in the Rat." Clinical Science 77, no. 1 (July 1, 1989): 77–84. http://dx.doi.org/10.1042/cs0770077.
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1. Experiments were performed upon anaesthetized rats to investigate the effect upon the initial 4 h of ischaemic acute renal failure of intrarenal flush with phosphate buffer (PB), sucrose alone and phosphate-buffered sucrose (PBS) solutions of differing compositions. 2. Kidneys flushed with PB immediately before 45 min pedicle clamp ischaemia exhibited a post-ischaemic function similar to that of control, non-flushed kidneys: they were isosthenuric and non-oliguric with a clearance of inulin (Cin) depressed to 10% of the pre-ischaemic value. 3. Kidneys flushed with 50 mmol/l sucrose in saline before ischaemia became isosthenuric, oliguric and had a more severely depressed post-ischaemic Cin compared with non-flushed kidneys. 4. Kidneys flushed with PBS containing either 50 (PBS50) or 140 (PBS140) mmol/l sucrose at pH 7 became polyuric after ischaemia, produced concentrated urine and had Cin values significantly higher than control kidneys. 5. Raising the pH of the PBS50 to 7.4 resulted in isosthenuric, polyuric kidneys that had a post-ischaemic Cin not significantly different from that of the control group. 6. It is concluded that the severity of the initial phase of ischaemic acute renal failure was significantly reduced by intrarenal flush with a PBS solution of pH 7; flush with PB or sucrose alone had no protective action.
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Mohite, Ajay A., Jennifer A. Perais, Philip McCullough, and Noemi Lois. "Retinal Ischaemia in Diabetic Retinopathy: Understanding and Overcoming a Therapeutic Challenge." Journal of Clinical Medicine 12, no. 6 (March 21, 2023): 2406. http://dx.doi.org/10.3390/jcm12062406.
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Background: Retinal ischaemia is present to a greater or lesser extent in all eyes with diabetic retinopathy (DR). Nonetheless, our understanding of its pathogenic mechanisms, risk factors, as well as other characteristics of retinal ischaemia in DR is very limited. To date, there is no treatment to revascularise ischaemic retina. Methods: Review of the literature highlighting the current knowledge on the topic of retinal ischaemia in DR, important observations made, and underlying gaps for which research is needed. Results: A very scarce number of clinical studies, mostly cross-sectional, have evaluated specifically retinal ischaemia in DR. Interindividual variability on its natural course and consequences, including the development of its major complications, namely diabetic macular ischaemia and proliferative diabetic retinopathy, have not been investigated. The in situ, surrounding, and distance effect of retinal ischaemia on retinal function and structure and its change over time remains also to be elucidated. Treatments to prevent the development of retinal ischaemia and, importantly, to achieve retinal reperfusion once capillary drop out has ensued, are very much needed and remain to be developed. Conclusion: Research into retinal ischaemia in diabetes should be a priority to save sight.
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Galante, Alberto, Antonio Pietroiusti, Bruno Domenici, Andrea Magrini, Sandro Carta, Francesco Colace, Luigi Dell' Uomo, et al. "Timing and Course of Leucocyte Aggregation in Myocardial Infarction." Thrombosis and Haemostasis 74, no. 05 (1995): 1221–24. http://dx.doi.org/10.1055/s-0038-1649915.
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SummaryIn order to evaluate the pathophysiological relevance and clinical implications of leukocyte rheology in myocardial ischaemia we measured the percentage of aggregated leukocytes in 43 subjects with acute substernal pain before diagnosis. The percentage of aggregated leukocytes was significantly higher in 16 patients with subsequent diagnosis of myocardial infarction with respect to 11 with angina and 16 with non ischaemic chest pain (4.75 ± 0.88, 3.43 ± 0.65 and 1.52 ±0.32 respectively p <0.01). The percentage of aggregated leukocytes was also evaluated in another group of 46 patients hospitalized for myocardial infarction. Among these, aggregated leukocytes were significantly higher in those with residual ischaemia, with respect to those without residual ischaemia (7.4 ± 1.1 vs 3.5 ±0.6, p <0.01).In conclusion, leukocyte aggregation is precociously increased after myocardial ischaemia. It may be a marker of residual ischaemia in patients with myocardial infarction.
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Zhang, Pei-Lei, Hai-Tao Lu, Jun-Gong Zhao, and Ming-Hua Li. "Protective effect of dl-3n-butylphthalide preconditioning on focal cerebral ischaemia-reperfusion injury in rats." Acta Neuropsychiatrica 25, no. 1 (February 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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Devereaux, P. J., and Wojciech Szczeklik. "Myocardial injury after non-cardiac surgery: diagnosis and management." European Heart Journal 41, no. 32 (May 16, 2019): 3083–91. http://dx.doi.org/10.1093/eurheartj/ehz301.
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Abstract Myocardial injury after non-cardiac surgery (MINS) is due to myocardial ischaemia (i.e. supply-demand mismatch or thrombus) and is associated with an increased risk of mortality and major vascular complications at 30 days and up to 2 years after non-cardiac surgery. The diagnostic criteria for MINS includes an elevated post-operative troponin measurement judged as resulting from myocardial ischaemia (i.e. no evidence of a non-ischaemic aetiology), during or within 30 days after non-cardiac surgery, and without the requirement of an ischaemic feature (e.g. ischaemic symptom, ischaemic electrocardiography finding). For patients with MINS who are not at high risk of bleeding, physicians should consider initiating dabigatran 110 mg twice daily and low-dose aspirin. Physicians should also consider initiating statin therapy in patients with MINS. Most MINS patients should only be referred to cardiac catheterization if they demonstrate recurrent instability (e.g. cardiac ischaemia, heart failure). Patients ≥65 years of age or with known atherosclerotic disease should have troponin measurements on days 1, 2, and 3 after surgery while the patient is in hospital to avoid missing >90% of MINS and the opportunity to initiate secondary prophylactic measures and follow-up.
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Hill, Bradford G., Sunday O. Awe, Elena Vladykovskaya, Yonis Ahmed, Si-Qi Liu, Aruni Bhatnagar, and Sanjay Srivastava. "Myocardial ischaemia inhibits mitochondrial metabolism of 4-hydroxy-trans-2-nonenal." Biochemical Journal 417, no. 2 (December 23, 2008): 513–24. http://dx.doi.org/10.1042/bj20081615.
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Myocardial ischaemia is associated with the generation of lipid peroxidation products such as HNE (4-hydroxy-trans-2-nonenal); however, the processes that predispose the ischaemic heart to toxicity by HNE and related species are not well understood. In the present study, we examined HNE metabolism in isolated aerobic and ischaemic rat hearts. In aerobic hearts, the reagent [3H]HNE was glutathiolated, oxidized to [3H]4-hydroxynonenoic acid, and reduced to [3H]1,4-dihydroxynonene. In ischaemic hearts, [3H]4-hydroxynonenoic acid formation was inhibited and higher levels of [3H]1,4-dihydroxynonene and [3H]GS-HNE (glutathione conjugate of HNE) were generated. Metabolism of [3H]HNE to [3H]4-hydroxynonenoic acid was restored upon reperfusion. Reperfused hearts were more efficient at metabolizing HNE than non-ischaemic hearts. Ischaemia increased the myocardial levels of endogenous HNE and 1,4-dihydroxynonene, but not 4-hydroxynonenoic acid. Isolated cardiac mitochondria metabolized [3H]HNE primarily to [3H]4-hydroxynonenoic acid and minimally to [3H]1,4-dihydroxynonene and [3H]GS-HNE. Moreover, [3H]4-hydroxynonenoic acid was extruded from mitochondria, whereas other [3H]HNE metabolites were retained in the matrix. Mitochondria isolated from ischaemic hearts were found to contain 2-fold higher levels of protein-bound HNE than the cytosol, as well as increased [3H]GS-HNE and [3H]1,4-dihydroxynonene, but not [3H]4-hydroxynonenoic acid. Mitochondrial HNE oxidation was inhibited at an NAD+/NADH ratio of 0.4 (equivalent to the ischaemic heart) and restored at an NAD+/NADH ratio of 8.6 (equivalent to the reperfused heart). These results suggest that HNE metabolism is inhibited during myocardial ischaemia owing to NAD+ depletion. This decrease in mitochondrial metabolism of lipid peroxidation products and the inability of the mitochondria to extrude HNE metabolites could contribute to myocardial ischaemia/reperfusion injury.
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Lindow, Thomas, Olle Pahlm, Charles W. Olson, Ardavan Khoshnood, Ulf Ekelund, Marcus Carlsson, Cees A. Swenne, Sumche Man, and Henrik Engblom. "Diagnostic Accuracy Of The Electrocardiographic Decision Support – Myocardial Ischaemia (EDS-MI) Algorithm In Detection Of Acute Coronary Occlusion." European Heart Journal: Acute Cardiovascular Care 9, no. 1_suppl (April 3, 2018): 13–25. http://dx.doi.org/10.1177/2048872618768081.
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Electrocardiographic Decision Support – Myocardial Ischaemia (EDS-MI) is a graphical decision support for detection and localization of acute transmural ischaemia. A recent study indicated that EDS-MI performs well for detection of acute transmural ischaemia. However, its performance has not been tested in patients with non-ischaemic ST-deviation. We aimed to optimize the diagnostic accuracy of EDS-MI in patients with verified acute coronary occlusion as well as patients with non-ischaemic ST deviation and compare its performance with STEMI criteria. We studied 135 patients with non-ischaemic ST deviation (perimyocarditis, left ventricular hypertrophy, takotsubo cardiomyopathy and early repolarization) and 117 patients with acute coronary occlusion. In 63 ischaemic patients, the extent and location of the ischaemic area (myocardium at risk) was assessed by both cardiovascular magnetic resonance imaging and EDS-MI. Sensitivity and specificity of ST elevation myocardial infarction criteria were 85% (95% confidence interval (CI) 77, 90) and 44% (95% CI 36, 53) respectively. Using EDS-MI, sensitivity and specificity increased to 92% (95% CI 85, 95) and 81% (95% CI 74, 87) respectively (p=0.035 and p<0.001). Agreement was strong (83%) between cardiovascular magnetic resonance imaging and EDS-MI in localization of ischaemia. Mean myocardium at risk was 32% (± 10) by cardiovascular magnetic resonance imaging and 33% (± 11) by EDS-MI when the estimated infarcted area according to Selvester QRS scoring was included in myocardium at risk estimation. In conclusion, EDS-MI increases diagnostic accuracy and may serve as an automatic decision support in the early management of patients with suspected acute coronary syndrome. The added clinical benefit in a non-selected clinical chest pain population needs to be assessed.
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Tian, Lin, Yunqian Li, Wei Hua, Ying Jia, Min Zhou, Yunhe Gu, and Jiping Qi. "Expression of Urotensin II During Focal Cerebral Ischemic in Diabetic Rats." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 41, no. 4 (July 2014): 498–503. http://dx.doi.org/10.1017/s0317167100018552.
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Background:The objective of this study was to explore the expression of urotensin II (UII), its receptor (GPR14), and vascular endothelial growth factor (VEGF), as well as their associations in the ischaemic brains of rats with focal cerebral ischaemia, under normal and diabetic conditions.Methods:Diabetes mellitus (DM) was induced by injection of streptozotocin (STZ) into Sprague—Dawley rats. Focal cerebral ischaemia was induced by middle cerebral artery occlusion (MCAO) four weeks after DM onset by STZ. Rats (n=80) were divided into four groups: normal control, DM, MCAO, and DM/MCAO. Immunohistochemistry and reverse-transcriptase-polymerase chain reaction (RT-PCR) were used to detect the expression of UII, GPR14 and VEGF in the diabetic and ischaemic brain.Results:Expression of UII and GPR14 was increased at mRNA and protein levels in the DM and MCAO group compared with controls. In the DM/MCAO group, expression of UII and GPR14 was increased significantly in the ischaemic brain, and was accompanied by a significantly increased VEGF expression.Conclusion:Diabetes mellitus was seen to aggravate brain lesions after ischaemia, and UII may have an important role.
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Fernandez-Sanz, Celia, José Castellano, Elisabet Miro-Casas, Estefanía Nuñez, Javier Inserte, Jesús Vázquez, David Garcia-Dorado, and Marisol Ruiz-Meana. "Altered FoF1 ATP synthase and susceptibility to mitochondrial permeability transition pore during ischaemia and reperfusion in aging cardiomyocytes." Thrombosis and Haemostasis 113, no. 03 (May 2015): 441–51. http://dx.doi.org/10.1160/th14-10-0901.
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SummaryAging is a major determinant of the incidence and severity of ischaemic heart disease. Preclinical information suggests the existence of intrinsic cellular alterations that contribute to ischaemic susceptibility in senescent myocardium, by mechanisms not well established. We investigated the role of altered mitochondrial function in the adverse effect of aging. Isolated perfused hearts from old mice (> 20 months) displayed increased ischaemia-reperfusion injury as compared to hearts from adult mice (6 months) despite delayed onset of ischaemic rigor contracture. In cardiomyocytes from aging hearts there was a more rapid decline of mitochondrial membrane potential (ΔΨm) as compared to young ones, but ischaemic rigor shortening was also delayed. Transient recovery of ΔΨm observed during ischaemia, secondary to the reversal of mitochondrial FoF1 ATP synthase to ATPase mode, was markedly reduced in aging cardiomyocytes. Proteomic analysis demonstrated increased oxidation of different subunits of ATP synthase. Altered bionergetics in aging cells was associated with reduced mitochondrial calcium uptake and more severe cytosolic calcium overload during ischaemia-reperfusion. Despite attenuated ROS burst and mitochondrial calcium overload, mitochondrial permeability transition pore (mPTP) opening and cell death was increased in reperfused aged cells. In vitro studies demonstrated a significantly reduced calcium retention capacity in interfibrillar mitochondria from aging hearts. Our results identify altered FoF1 ATP synthase and increased sensitivity of mitochondria to undergo mPTP opening as important determinants of the reduced tolerance to ischaemia-reperfusion in aging hearts. Because ATP synthase has been proposed to conform mPTP, it is tempting to hypothesise that oxidation of ATP synthase underlie both phenomena.
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WACHTEL, Marco, Karl FREI, Elisabeth EHLER, Christian BAUER, Max GASSMANN, and Sergio M. GLOOR. "Extracellular signal-regulated protein kinase activation during reoxygenation is required to restore ischaemia-induced endothelial barrier failure." Biochemical Journal 367, no. 3 (November 1, 2002): 873–79. http://dx.doi.org/10.1042/bj20020746.
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During an ischaemic insult, oedema formation occurs as a consequence of increased vascular permeability. To study mechanisms leading to vascular barrier failure, endothelial cells were exposed to ischaemia (1% O2 in serum- and glucose-free medium) for 5h. In in vitro conditions, ischaemia increased paracellular permeability, disassembled actin stress fibres, displaced focal adhesion kinase (FAK) from focal adhesions and enhanced cytoskeletal association of occludin. Reoxygenation restored paracellular barrier function, actin organization and FAK distribution. The mitogen-activated protein kinase (MAPK)/extracellular signal-regulated protein kinase (ERK) was rapidly activated after 30min, strongly inhibited after 5h of continuous ischaemia and reactivated 3 times more than control during reoxygenation. Inhibition of ERK activation during reoxygenation with U0126, an inhibitor of the ERK activator, MAPK/ERK kinase 1/2, prevented both barrier restoration and stress-fibre formation, but did not prevent recruitment of FAK to focal contacts. Under normoxic conditions, ERK inhibition led to barrier failure and disassembly of stress fibres only in the absence of serum. These results demonstrate that ERK activity is essential to rebuild a disrupted endothelial barrier after ischaemia and to maintain barrier function in cells exposed to non-ischaemic stress.
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O'Shaughnessy, C. T., N. J. Rothwell, and J. Shrewsbury-Gee. "Effects of an analogue of thyrotrophin-releasing hormone, RX77368, on infarct size and cerebral blood flow in focal cerebral ischaemia in the rat." Canadian Journal of Physiology and Pharmacology 67, no. 10 (October 1, 1989): 1345–50. http://dx.doi.org/10.1139/y89-214.
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Effects of a stable analogue of thyrotrophin-releasing hormone, RX77368, on cerebral blood flow and infarct size have been studied in an acute model of cerebral ischaemia in the rat. Two hours after electrocoagulation of the left middle cerebral artery (MCA), the mean area of ischaemia (± SEM), determined histochemically, was 11.5 ± 2.2% of a single hemisphere and blood flow, determined using radiolabeled microspheres, was reduced by 40% in the left forebrain (p < 0.001 compared with sham-operated animals). Administration of RX77368 (50 μg/kg, intracerebroventricularly) within 10 min of arterial occlusion caused a significant (p < 0.01) reduction in mean lesion size to 3.7 ± 1.8% and stimulation of blood flow to the left ischaemic forebrain (60% above saline treated). Peripheral administration of RX77368 (1 mg/kg intraperitoneally) also significantly stimulated blood flow to the ischaemic forebrain and caused an apparent decrease in frequency of large infarcted areas of brain tissue, although mean lesion size was not significantly affected. These findings indicate that RX77368 ameliorates tissue damage in acute focal cerebral ischaemia. Such effects may be related to stimulation of cerebral blood flow.Key words: middle cerebral artery, focal cerebral ischaemia, cerebral blood flow, thyrotrophin-releasing hormone analogue.
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MARTÍN, M. Elena, Francisco M. MUÑOZ, Matilde SALINAS, and Juan L. FANDO. "Ischaemia induces changes in the association of the binding protein 4E-BP1 and eukaryotic initiation factor (eIF) 4G to eIF4E in differentiated PC12 cells." Biochemical Journal 351, no. 2 (October 10, 2000): 327–34. http://dx.doi.org/10.1042/bj3510327.
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Ischaemia was obtained in vitro by subjecting nerve-growth-factor-differentiated PC12 cells to glucose deprivation plus anoxia. During ischaemia the rate of protein synthesis was significantly inhibited, and eIF4E-binding protein (4E-BP1) and eukaryotic initiation factor 4E (eIF4E) were significantly dephosphorylated in parallel. In addition, ischaemia induced an enhancement of the association of 4E-BP1 to eIF4E, which in turn decreased eIF4F formation, whereas no degradation of initiation factor 4G was observed. The treatment of PC12 cells with the specific p38 mitogen-activated protein kinase inhibitor SB203580 induced eIF4E dephosphorylation but did not cause any effect on protein synthesis rate. Rapamycin, the inhibitor of mammalian target of rapamycin (‘mTOR’), but not PD98059, the inhibitor of extracellular signal-regulated protein kinases (‘ERK1/2’), induced similar effects on 4E-BP1 phosphorylation to ischaemia; nevertheless, 4E-BP1–eIF4E complex levels were higher in ischaemia than in rapamycin-treated cells. In addition, both protein synthesis rate and eIF4F formation were lower in ischaemic cells than in rapamycin-treated cells.
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Ozkisacik, Sezen, Ali Onur Erdem, Barlas Etensel, Canten Tataroglu, Mukadder Serter, and Mesut Yazici. "Short-interval postconditioning protects the bowel against ischaemia–reperfusion injury in rats." Journal of International Medical Research 45, no. 3 (May 28, 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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Schuenemann, G. M., S. M. L. C. Mendis-Handagama, T. M. Prado, and F. N. Schrick. "Alteration in testicular cell components following transiently induced ischaemia in prepubertal bulls." Reproduction, Fertility and Development 20, no. 7 (2008): 826. http://dx.doi.org/10.1071/rd08003.
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The aim of the present study was to evaluate transient testicular ischaemia (induced using elastrator bands) in Jersey calves on testicular morphology and development. Treatments (at 27 ± 5 days of age) consisted of control (0 h banding) and banding for 2, 4 or 8 h (n = 4 in each group). After castration (at 60 ± 5 days of age), the right testis was used for calculation of cell components per testis according to the point-counting method. Bodyweight (59.8 ± 6.2 kg) and scrotal circumference (SC) at banding (9.1 ± 0.2 cm) did not differ between groups. Fresh testis weight, scrotal temperature immediately before band removal and daily SC growth were decreased in ischaemic (4 and 8 h) testes compared with controls (P < 0.05). In addition, the number of Sertoli and Leydig cells was significantly reduced in the 8 h ischaemic treatment group (P < 0.05). Transiently induced ischaemia significantly decreased the number of germ cells in the 8 h ischaemic treatment group (13 ± 5 × 106 cells) compared with the 0, 2 and 4 h ischaemic treatment groups (38 ± 6, 32 ± 6 and 33 ± 5 × 106 cells, respectively; P < 0.05). These results suggest that transiently induced ischaemia for 8 h significantly decreases the number of germ, Sertoli and Leydig cells in prepubertal testis.
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van de POLL, Marcel C. G., Cornelis H. C. Dejong, Marc A. J. G. Fischer, Aalt Bast, and Ger H. Koek. "Decreased hepatosplanchnic antioxidant uptake during hepatic ischaemia/reperfusion in patients undergoing liver resection." Clinical Science 114, no. 8 (March 13, 2008): 553–60. http://dx.doi.org/10.1042/cs20070317.
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Oxidative stress mediates cell injury during ischaemia/reperfusion. On the other hand, experimental findings suggest that ROS (reactive oxygen species) induce processes leading to ischaemic preconditioning. The extent and source of oxidative stress and its effect on antioxidant status in the human liver during intermittent ischaemia and reperfusion remains ill-defined. Therefore the aim of the present study was to investigate the occurrence of oxidative stress in humans undergoing liver resection. Liver biopsies, and arterial and hepatic venous blood samples were taken from ten patients undergoing hepatectomy with an intermittent Pringle manoeuvre. Plasma MDA (malondialdehyde) and hepatic GSSG levels were measured as markers of oxidative stress and plasma uric acid as a marker of xanthine oxidase activity. In addition, changes in hepatosplanchnic consumption of plasma antioxidants and hepatic levels of carotenoids and glutathione (GSH) were measured. After ischaemia, hepatosplanchnic release of MDA and increased hepatic GSSG levels were found. This was accompanied by the release of uric acid, reflecting xanthine oxidase activity. During reperfusion, ongoing oxidative stress was observed by further increases in hepatic GSSG content and hepatosplanchnic MDA release. Uric acid release was minimal during reperfusion. A gradual decrease in plasma antioxidant capacity and net hepatosplanchnic antioxidant uptake was observed upon prolonged cumulative ischaemia. Oxidative stress occurs during hepatic ischaemia in man mainly due to xanthine oxidase activity. Interestingly, the gradual decline in plasma antioxidant capacity and net hepatosplanchnic antioxidant uptake during prolonged cumulative ischaemia, preserved both hydrophilic and lipophilic hepatic antioxidant levels. Decreasing plasma levels and net hepatosplanchnic uptake of plasma antioxidants may warrant antioxidant supplementation, although it should be clarified to what extent limitation of oxidative stress compromises ROS-dependent pathways of ischaemic preconditioning.
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DAS, D. K. "Ischaemic preconditioning and myocardial adaptation to ischaemia." Cardiovascular Research 27, no. 11 (November 1, 1993): 2077–79. http://dx.doi.org/10.1093/cvr/27.11.2077.
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Herron, Caroline, Conn L. Hastings, Clodagh Herron-Rice, Helena M. Kelly, Joanne O’Dwyer, and Garry P. Duffy. "A Thermoresponsive Chitosan/β-Glycerophosphate Hydrogel for Minimally Invasive Treatment of Critical Limb Ischaemia." Polymers 13, no. 20 (October 16, 2021): 3568. http://dx.doi.org/10.3390/polym13203568.
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A reduction in blood supply to any limb causes ischaemia, pain and morbidity. Critical limb ischaemia is the most serious presentation of peripheral vascular disease. One in five patients with critical limb ischaemia will die within six months of diagnosis and one in three will require amputation in this time. Improving blood flow to the limb, via the administration of angiogenic agents, could relieve pain and avoid amputation. Herein, chitosan is combined with β-glycerophosphate to form a thermoresponsive formulation (chitosan/β-GP) that will flow through a syringe and needle at room temperature but will form a gel at body temperature. The chitosan/β-GP hydrogel, with or without the angiogenic molecule desferrioxamine (DFO), was injected into the mouse hind limb, following vessel ligation, to test the ability of the formulations to induce angiogenesis. The effects of the formulations were measured using laser Doppler imaging to determine limb perfusion and CD31 staining to quantify the number of blood vessels. Twenty-eight days following induction of ischaemia, the chitosan/β-GP and chitosan/β-GP + 100 µM DFO formulations had significantly (p < 0.001 and p < 0.05, respectively) improved blood flow in the ischaemic limb compared with an untreated control. Chitosan/β-GP increased vessel number by 1.7-fold in the thigh of the ischaemic limb compared with an untreated control, while chitosan/β-GP + 100 µM DFO increased vessel number 1.8-fold. Chitosan/β-GP represents a potential minimally invasive treatment for critical limb ischaemia.
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Timmis, Adam, Antony Raharja, R. Andrew Archbold, and Anthony Mathur. "Validity of inducible ischaemia as a surrogate for adverse outcomes in stable coronary artery disease." Heart 104, no. 21 (June 6, 2018): 1733–38. http://dx.doi.org/10.1136/heartjnl-2018-313230.
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Regional myocardial ischaemia is commonly expressed as exertional angina in patients with stable coronary artery disease (CAD). It also associates with prognosis, risk tending to increase with the severity of ischaemia. The validity of myocardial ischaemia as a surrogate for adverse clinical outcomes, however, has not been well established. Thus, in cohort studies, ischaemia testing has failed to influence rates of myocardial infarction and coronary death. Moreover, in clinical studies, pharmacological and interventional treatments that are effective in correcting ischaemia have rarely been shown to reduce cardiovascular (CV) risk. This contrasts with statins and other anti-inflammatory drugs that have no direct effect on ischaemia but improve CV outcomes by modifying the atherothrombotic disease process. Despite this, and with little evidence of patient benefit, stress testing is commonly used during the follow-up of patients with stable CAD when the demonstration of ischaemic change may be seen as a target for treatment, independently of symptomatic status. Substitution of a symptom-driven management strategy has the potential to reduce rates of non-invasive stress testing, unnecessary downstream revascularisation procedures and use of valuable resources in patients with stable CAD without adverse consequences for CV risk.
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Nedvig, Klára, István Zapf, and Tamás Fekecs. "A vékonybél meleg és hideg ischaemiás károsodásának kimutatása differenciál pásztázó kalorimetriás vizsgálattal." Magyar Sebészet 64, no. 4 (August 1, 2011): 207–12. http://dx.doi.org/10.1556/maseb.64.2011.4.5.
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Absztrakt Bevezetés/célkitűzés: Annak ténye, hogy a vékonybél rendkívül érzékeny az ischaemiás/reperfusiós károsodásokra, indította el azokat az összehasonlító vizsgálatokat, ahol meleg és hideg ischaemia hatására a bél szöveti struktúrájában bekövetkező változásokat tanulmányoztuk differenciál pásztázó kalorimetriás (DSC) módszerrel. Anyag és módszerek: Meleg és hideg ischaemiás csoportokat hoztunk létre 1, 3 és 6 órás ischaemiás időkkel Wistar-patkányokon (n = 30). A bélszövetből mintát vettünk a laparotomia után (kontroll) és az ischaemiás periódusok végén. A DSC méréseket a bél mucosa- és izomrétegén, valamint a teljes bélfal mintáiban végeztük el. Eredmények: A DSC adatok megerősítették, hogy a meleg ischaemia idejének növelése fokozza a mucosa- és izomréteg károsodását. Az átalakulási hőmérséklet és a kalorimetriás entalpia eredmények alapján úgy tűnik, hogy a károsodás kisebb mértékű University of Wisconsin oldatban történő hideg tárolás esetén, de a bélszövet valamennyi rétegében bekövetkező termikus destructio jelzi, hogy jelentős károsodás áll fenn. Következtetések: Jelen munkánkban DSC technikával kvantitatív módon tudtuk kimutatni az ischaemia hatására a bélszövetben bekövetkező strukturális károsodásokat. Ez a termoanalitikai módszer alkalmasnak tűnik a jövőben további különböző stresszmodellek vizsgálatára.
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Lin, Song, Yan Chen, Yongxue Li, Jianan Li, and Xiao Lu. "Physical ischaemia induced by isometric exercise facilitated collateral development in the remote ischaemic myocardium of humans." Clinical Science 127, no. 10 (July 18, 2014): 581–88. http://dx.doi.org/10.1042/cs20130618.
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Isometric-handgrip-exercise-induced local ischaemia in the normal limb facilitated collateral recruitment in acutely occluded vessels in patients with coronary artery disease. Ischaemic-handgrip-exercise-induced physical ischaemic training for 3 months facilitated myocardial collateral growth.
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Zhang, Ya-Jun, Wen-Jing Guo, Zi-Yuan Tang, Hong-Bin Lin, Pu Hong, Jing-Wei Wang, Xuan-Xuan Huang, Feng-Xian Li, Shi-Yuan Xu, and Hong-Fei Zhang. "Isoflurane Attenuates Cerebral Ischaemia–Reperfusion Injury via the TLR4-NLRP3 Signalling Pathway in Diabetic Mice." Oxidative Medicine and Cellular Longevity 2022 (April 4, 2022): 1–16. http://dx.doi.org/10.1155/2022/2650693.
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Ischaemic stroke is a severe disease worldwide. Restoration of blood flow after ischaemic stroke leads to cerebral ischaemia–reperfusion injury (CIRI). Various operations, such as cardiac surgery with deep hypothermic circulatory arrest, predictably cause cerebral ischaemia. Diabetes is related to the occurrence of perioperative stroke and exacerbates neurological impairment after stroke. Therefore, the choice of anaesthetic drugs has certain clinical significance for patients with diabetes. Isoflurane (ISO) exerts neuroprotective and anti-neuroinflammatory effects in patients without diabetes. However, the role of ISO in cerebral ischaemia in the context of diabetes is still unknown. Toll-like receptor 4 (TLR4) and NOD-like receptor pyrin domain-containing protein 3 (NLRP3) inflammasome activation play important roles in microglia-mediated neuroinflammatory injury. In this study, we treated a diabetic middle cerebral artery occlusion mouse model with ISO. We found that diabetes exacerbated cerebral ischaemia damage and that ISO exerted neuroprotective effects in diabetic mice. Then, we found that ISO decreased TLR4-NLRP3 inflammasome activation in microglia and the excessive autophagy induced by CIRI in diabetic mice. The TLR4-specific agonist CRX-527 reversed the neuroprotective effects of ISO. In summary, our study indicated that ISO exerts neuroprotective effects against the neuroinflammation and autophagy observed during diabetic stroke via the TLR4-NLRP3 signalling pathway.
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Martinez-Navarro, Hector, Xin Zhou, Alfonso Bueno-Orovio, and Blanca Rodriguez. "Electrophysiological and anatomical factors determine arrhythmic risk in acute myocardial ischaemia and its modulation by sodium current availability." Interface Focus 11, no. 1 (December 11, 2020): 20190124. http://dx.doi.org/10.1098/rsfs.2019.0124.
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Acute myocardial ischaemia caused by coronary artery disease is one of the main causes of sudden cardiac death. Even though sodium current blockers are used as anti-arrhythmic drugs, decreased sodium current availability, also caused by mutations, has been shown to increase arrhythmic risk in ischaemic patients. The mechanisms are still unclear. Our goal is to exploit perfect control and data transparency of over 300 high-performance computing simulations to investigate arrhythmia mechanisms in acute myocardial ischaemia with variable sodium current availability. The human anatomically based torso-biventricular electrophysiological model used includes representation of realistic ventricular anatomy and fibre architecture, as well as ionic to electrocardiographic properties. Simulations show that reduced sodium current availability increased arrhythmic risk in acute regional ischaemia due to both electrophysiological (increased dispersion of refractoriness across the ischaemic border zone) and anatomical factors (conduction block from the thin right ventricle to thick left ventricle). The asymmetric ventricular anatomy caused high arrhythmic risk specifically for ectopic stimuli originating from the right ventricle and ventricular base. Increased sodium current availability was ineffective in reducing arrhythmic risk for septo-basal ectopic excitation. Human-based multiscale modelling and simulations reveal key electrophysiological and anatomical factors determining arrhythmic risk in acute ischaemia with variable sodium current availability.
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Szijártó, Attila, Zsolt Turóczi, Péter Arányi, Dávid Garbaisz, Márk Varga, Rita Stangl, Gábor Lotz, and Péter Kupcsulik. "Hosszú idejű végtagi verőér-elzáródás és izomszövet-életképesség vizsgálata kísérletes állatmodellben." Magyar Sebészet 63, no. 6 (December 1, 2010): 374–79. http://dx.doi.org/10.1556/maseb.63.2010.6.4.
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Absztrakt Bevezetés: Az acut végtagi ischaemiás események kezelése stádiumtól függően revascularisatio vagy amputáció. A végső irreverzibilis károsodást jelentő stádium elkülönítése azonban jelen ismereteink alapján nem egyértelmű. Célkitűzés: Acut, hosszú idejű verőér-elzáródások vizsgálata állatkísérletesen, illetve a posztkondicionálás alkalmazhatóságának megítélése hosszú idejű ischaemiát követően. Anyagok és módszerek: I. kísérlet: hím Wistar-patkányokon infrarenalis aortakirekesztést követően 4, 6 és 8 órás ischaemia került létrehozásra reperfusio nélkül. II. kísérlet: az irreverzibilisnek vélt ischaemiát 2 óra reperfusio követte, az egyik csoportban posztkondicionálás történt. Mindkét kísérlet során izomszövettani mintavétel történt rutin szövettani, valamint nitroblue-tetrazolium enzim-hisztokémiai vizsgálatok céljából. A második kísérlet során a microcirculatiós változások Laser Doppler Flowmeterrel (LDF) kerültek regisztrálásra, valamint kreatin-kináz-meghatározás történt. Eredmények: I. kísérlet: 8 órás kirekesztést követően a morfológiai, valamint az enzim-hisztokémiai vizsgálatok irreverzibilis károsodást jeleztek. II. kísérlet: A súlyosan csökkent életképesség és microcirculatiós eredmények megerősítik az irreverzibilitást a 8 órás ischaemia után. A posztkondicionált csoport izomrostjainak életképessége szignifikánsan magasabbnak mutatkozott (p < 0,001), a microcirculatio reperfusiót jellemző paraméterei szignifikáns javulást mutattak (p < 0,05), valamint a szérum-kreatin-kináz-szintek szignifikánsan alacsonyabbak voltak (p < 0,05) a kontrollhoz képest. Következtetés: A 8 óra kirekesztés irreverzibilis károsodáshoz vezethet patkányban. A posztkondicionálás javasolható eljárás az acut végtagi verőér-elzáródások által okozott károsodás mérséklésére.
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Myrtek, M., E. Frölich, A. Fichtler, and G. Brügner. "ECG Changes, Emotional Arousal, and Subjective State." Journal of Psychophysiology 14, no. 2 (April 2000): 106–14. http://dx.doi.org/10.1027//0269-8803.14.2.106.
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Abstract Laboratory studies with CHD patients suggest an adverse influence of emotional/mental arousal on myocardial ischaemia or ventricular premature contractions (VPCs). However, it is controversial whether such studies can be generalized to everyday life. In addition, existing ambulatory monitoring studies have shortcomings because emotional arousal is entirely based on subjective reports. The hypothesis of the present study is that during ischaemic episodes or VPCs “objective emotional/mental arousal” will be more pronounced than during comparable episodes without these events. Objective emotional/mental arousal was indicated by a special ambulatory monitoring method which was based on the online analysis of heart rate and physical activity, resulting in the so-called emotional or non-metabolic heart rate. Moreover, the method allowed for ratings of anginal pain. In 223 CHD patients the associations between ischaemia, VPCs, objective emotional/mental arousal, and anginal pain were investigated. Forty-nine patients revealed ischaemic episodes and 115 patients VPCs. Emotional/mental arousal was higher during ischaemic episodes as compared to control minutes whereas minutes with VPCs showed no difference. No differences between ischaemic episodes or VPCs and the respective control minutes were observed for anginal pain. Objective emotional/mental arousal was associated in this study with ischaemia but not with arrhythmia, thus partly confirming the hypothesis stated. Because anginal pain was not related to objective cardiac events, detection of CHD has to rely on medical examinations.
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Cabrera-Fuentes, Hector, Isabel Steinert, Klaus Preissner, Péter Bencsik, Márta Sárközy, Csaba Csonka, Péter Ferdinandy, et al. "Mechanism and consequences of the shift in cardiac arginine metabolism following ischaemia and reperfusion in rats." Thrombosis and Haemostasis 113, no. 03 (May 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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Miller, Robert J. H., Lien-Hsin Hu, Heidi Gransar, Julian Betancur, Evann Eisenberg, Yuka Otaki, Tali Sharir, et al. "Transient ischaemic dilation and post-stress wall motion abnormality increase risk in patients with less than moderate ischaemia: analysis of the REFINE SPECT registry." European Heart Journal - Cardiovascular Imaging 21, no. 5 (July 13, 2019): 567–75. http://dx.doi.org/10.1093/ehjci/jez172.
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Abstract Aims Ischaemia on single-photon emission computed tomography (SPECT) myocardial perfusion imaging (MPI) is strongly associated with cardiovascular risk. Transient ischaemic dilation (TID) and post-stress wall motion abnormalities (WMA) are non-perfusion markers of ischaemia with incremental prognostic utility. Using a large, multicentre SPECT MPI registry, we assessed the degree to which these features increased the risk of major adverse cardiovascular events (MACE) in patients with less than moderate ischaemia. Methods and results Ischaemia was quantified with total perfusion deficit using semiautomated software and classified as: none (<1%), minimal (1 to <5%), mild (5 to <10%), moderate (10 to <15%), and severe (≥15%). Univariable and multivariable Cox proportional hazard analyses were used to assess associations between high-risk imaging features and MACE. We included 16 578 patients, mean age 64.2 and median follow-up 4.7 years. During follow-up, 1842 patients experienced at least one event. Patients with mild ischaemia and TID were more likely to experience MACE compared with patients without TID [adjusted hazard ratio (HR) 1.42, P = 0.023], with outcomes not significantly different from patients with moderate ischaemia without other high-risk features (unadjusted HR 1.15, P = 0.556). There were similar findings in patients with post-stress WMA. However, in multivariable analysis of patients with mild ischaemia, TID (adjusted HR 1.50, P = 0.037), but not WMA, was independently associated with increased MACE. Conclusion In patients with mild ischaemia, TID or post-stress WMA identify groups of patients with outcomes similar to patients with moderate ischaemia. Whether these combinations identify patients who may derive benefit from revascularization deserves further investigation.
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Sharma, Rajan, David C. Gaze, Denis Pellerin, Rajnikant L. Mehta, Helen Gregson, Christopher P. Streather, Paul O. Collinson, and Stephen J. D. Brecker. "Evaluation of ischaemia-modified albumin as a marker of myocardial ischaemia in end-stage renal disease." Clinical Science 113, no. 1 (June 1, 2007): 25–32. http://dx.doi.org/10.1042/cs20070015.
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The early diagnosis of myocardial ischaemia is problematic in patients with ESRD (end-stage renal disease). The aim of the present study was to determine whether IMA (ischaemia-modified albumin) increases during dobutamine stress and detects myocardial ischaemia in patients with ESRD. A total of 114 renal transplant candidates were studied prospectively, and all received DSE (dobutamine stress echocardiography). IMA levels were taken at baseline and 1 h after cessation of DSE. A total of 35 patients (31%) had a positive DSE result. Baseline IMA levels were not significantly different in the DSE-positive and -negative groups. The increase in IMA was significantly higher in the DSE-positive group compared with those with no ischaemic response (26.5±19.1 compared with 8.2±9.6 kU/l respectively; P=0.007; where kU is kilo-units). From ROC (receiver operator charactertistic) curve analysis, the optimal IMA increase to predict an ischaemic response was 20 kU/l, with a sensitivity of 81% and a specificity of 72% [area under the curve, 0.80 (95% confidence interval, 0.44–0.94); P=0.03]. There were 18 deaths, ten of which were cardiac in nature over a follow up period of 2.25±0.71 years. An increase in IMA ≥20 kU/l was associated with significantly worse survival (P=0.02). In conclusion, IMA is a moderately accurate marker of myocardial ischaemia in ESRD. Patients with an increase in IMA ≥20 kU/l during DSE had significantly worse survival.
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Zhang, Shengxiang. "Microglial activation after ischaemic stroke." Stroke and Vascular Neurology 4, no. 2 (May 10, 2019): 71–74. http://dx.doi.org/10.1136/svn-2018-000196.
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Ischaemic stroke can induce rapid activation of microglia. As the resident immune cells of the central nervous system, microglial activation is believed to play a central role in neuroinflammation and pathological progression of ischaemic tissue. The activation of microglia after ischaemia involves several stereotypical events including morphological transformation, proliferation and polarisation. Studies using confocal or two-photon imaging techniques have revealed that the degree of microglial activation is correlated with the degree of ischaemia. Activated microglia display diverse polarisation phenotypes. It remains largely unclear regarding whether activated microglia are beneficial or detrimental to poststroke recovery. This mini-review focuses on the morphological and functional aspects of microglial activation, with particular attention to progress in two-photon imaging studies.