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1
Content available remote

Comparison of the efficiency of Na+/Ca2+ exchanger or Na+/H+ exchanger inhibition and their combination in reducing coronary reperfusion-induced arrhythmias

100%
Szepesi J., Acsai K., Sebok Z., Prorok J., Pollesello P., Levijoki J., Papp J. G., Varro A., Toth A.
Journal of Physiology and Pharmacology
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2015
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tom 66
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nr 2
2
Content available remote

Hypercholesterolemia antagonized heart adaptation and functional remodeling of the mitochondria observed in acute diabetes mellitus subjected to ischemia/reperfusion injury

100%
Ferko M., Farkasova V., Jasova M., Kancirova I., Ravingerova T., Duris Adameova A., Andelova N., Waczulikova I.
Journal of Physiology and Pharmacology
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2018
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tom 69
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nr 5
3
Content available remote

Pharmacological caspase inhibitors: research towards therapeutic perspectives

100%
Kudelova J., Fleischmannova J., Adamova E., Matalova E.
Journal of Physiology and Pharmacology
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2015
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tom 66
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nr 4
4

Monocytes in sterile inflammation: recruitment and functional consequences

100%
Spahn J. H., Kreisel D.
Archivum Immunologiae et Therapiae Experimentalis
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2014
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tom 62
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nr 3
5

In vivo cardioprotective effects and pharmacokinetic profile of N-propyl caffeamide against ischemia reperfusion injury

84%
Cheng Y.-Y., Luo D., Xia Z., Tse H.-F., Li X., Rong J.
Archivum Immunologiae et Therapiae Experimentalis
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2017
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tom 65
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nr 2
6
Content available remote

The influence of the low-energy defibrillating impulse on the endothelin-1 concentration in the left heart ventricle and blood serum of the healthy rabbits

84%
Zurawinski W., Kokot T., Swietochowska E., Sosada K., Muc-Wierzgon M.
Journal of Physiology and Pharmacology
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2019
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tom 70
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nr 1
7

Decreased serum level of IL-12 in the course of ischemia and reperfusion during abdominal aortic surgery

67%
Jedynak M., Mroczko B., Siemiatkowski A., Gacko M., Szmitkowski M.
Folia Histochemica et Cytobiologica
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2011
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tom 49
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nr 3
8

Influence of infliximab pretreatment on ischemia/reperfusion injury in rat intestine

67%
Akdogan R. A., Kalkan Y., Tumkaya L., Alacam H., Erdivanli B., Aydin I.
Folia Histochemica et Cytobiologica
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2014
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tom 52
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nr 1
9

Hydrogen gas reduces brain injury in a global cerebral ischemia model

67%
Ostrowski R. P., Mansell C., Zhang J. H.
Acta Neurobiologiae Experimentalis
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2013
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tom 73
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nr 1
Transient global cerebral ischemia-reperfusion injury can occur during acute severe hypotensive states and in cardiac arrest that is followed by resuscitation. This transient reduction in perfusion causes an insult to selective hippocampal neuronal populations via an apoptotic mechanism. Hydrogen gas has a neuroprotective effect and could be used as a pharmacologic agent of beneficial effect. As such we set out in this study to describe the effect of the inhalation of 2.9% hydrogen enriched air following an ischemia-reperfusion injury. A 2-vessel occlusion model was used to induce global cerebral ischemia for 6 minutes while maintaining a hypotensive state with a mean arterial pressure of 30 mm Hg through reversible exsanguinations in male Sprague-Dawley rats (280–330 g). The study included three groups: global ischemia without treatment (GI, n=6), global ischemia with hydrogen (GI + H2, n=6 ) and sham surgery (Sham, n=6). Rats in the treatment group received 2.9% inhalational hydrogen for 1 hour starting 15 minutes following reperfusion. Neurobehavioral testing was performed on day one and T-maze testing prior to being euthanized on days 3 or 7. Treated rats demonstrated an improved outcomes in spontaneous alternations, seizure incidence and survivability. Quantitative Nissl histology and TUNEL of the CA-1 region of the hippocampus showed increased cell survival in the treatment group. We conclude that treatment with inhalational hydrogen following ischemia-reperfusion injury could be low cost method of decreasing the effects of neuronal cell death.
10
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Administration of low doses of tumor necrosis factor-alpha protects rat liver from ischaemic damage and reperfusion injury

67%
Helewski K. J., Kowalczyk-Ziomek G. I., Czecior E., Swietochowska E., Wielkoszynski T., Czuba Z. P., Szliszka E., Krol W.
Journal of Physiology and Pharmacology
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2010
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tom 61
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nr 3
273-278
Liver ischaemia and reperfusion (IR) injury is a significant clinical problem. The aim of our study was to investigate the protective effect of tumor necrosis factor-alpha (TNF-) on rat liver ischaemia-reperfusion injury. A TNF- dose of 3 µg/kg body weight was injected into rats that had undergone partial (70%) ischaemia and reperfusion. The activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST), total blood antioxidant level (using the FRAP test), and the concentrations of TNF-, myeloperoxidase (MPO) and malondialdehyde (MDA) in liver homogenates after 1, 6, and 72 hours of reperfusion were measured. It was demonstrated that, rats subjected to IR, the administration of small doses of TNF- significantly reduced ALT and AST activities after 60- minute liver ischaemia and 1 or 6 hour of reperfusion. The strongest reductions in ALT and AST activities were seen after 1 hour of reperfusion (30% and 35%, respectively). Exogenous TNF- reduced the release of this cytokine in all observed periods, with the greatest reduction observed after 1 hour of reperfusion. Decreases in MPO concentration (by 40-45% in all periods of observation), as a marker of hepatic neutrophil infiltration, and in MDA concentration, the end-product of lipid peroxidation (by 55-60% at all time points), accompanied the reduction of TNF- release. The administration of TNF- to the rats after IR did not alter total plasma antioxidant potential, as assayed by the FRAP test, after 1 hour of reperfusion; however, at the later times a marked increase (~ 40-50%) occurred. We demonstrated that intraperitoneal injections of small doses of TNF- protect rat livers from IR injury. The mechanism of this protection is related to reductions in the release of TNF- during IR after injection of this cytokine, resulting in reductions in oxidative stress and inflammation during the later phase of reperfusion.
11
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The prevention of ischemia/reperfusion induced oxidative damage by venous blood in rabbit kidneys monitored with biochemical, histopathological and immunohistochemical analysis

67%
Cetin N., Suleyman H., Sener E., Demirci E., Gundogdu C., Akcay F.
Journal of Physiology and Pharmacology
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2014
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tom 65
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nr 3
12
Content available remote

Emerging roles of proteasomes in ischemia-reperfusion injury of organs

67%
Kukan M.
Journal of Physiology and Pharmacology
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2004
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tom 55
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nr 1,1
Proteasomes are the main non-lysosomal, multicatalytic proteinase complexes involved in the degradation of most intracellular proteins and in numerous cell processes. Studies from isolated cell models indicate that agents that induce oxidative stress may also damage proteasomes. Similarly, continuous oxidative stress during cell aging may impair proteasome activity. In ischemia-reperfusion models of organ injury, proteasomes may be involved in several ways. First, proteasomes were found to be targets of ischemia-reperfusion injury of the brain and heart. Second, proteasome activity increased in liver models of ischemia-reperfusion. Third, proteasome inhibition prevented ischemia-reperfusion injury of the brain, heart and kidney. A major mechanism by which proteasome inhibititors may confer tissue protection is inactivation of transcription activator nuclear factor-B resulting in a block of expression of cytokines and cell adhesion molecules during the reperfusion phase. Thus, proteasome inhibition represents a novel strategy for the treatment of pathologies such as stroke, infarction, and kidney failure.
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