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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Chytilová, A. Borchert, G. H. Mandíková-Alánová, P. Hlavácková, M. Kopkan, L. Khan, Md A. Hye Imig, J. D. Kolár, F. Neckár, J. |
| Description | Country affiliation: Czech Republic Author Affiliation: Chytilová A ( Institute of Physiology, The Czech Academy of Sciences, Prague, Czech Republic) |
| Abstract | AIM: It has been demonstrated that tumour necrosis factor-alpha (TNF- ) via its receptor 2 (TNFR2) plays a role in the cardioprotective effects of preconditioning. It is also well known that chronic hypoxia is associated with activation of inflammatory response. With this background, we hypothesized that TNF- signalling may contribute to the improved ischaemic tolerance of chronically hypoxic hearts. METHODS: Adult male Wistar rats were kept either at room air (normoxic controls) or at continuous normobaric hypoxia (CNH; inspired O2 fraction 0.1) for 3 weeks; subgroups of animals were treated with infliximab (monoclonal antibody against TNF- ; 5 mg kg(-1), i.p., once a week). Myocardial levels of oxidative stress markers and the expression of selected signalling molecules were analysed. Infarct size (tetrazolium staining) was assessed in open-chest rats subjected to acute coronary artery occlusion/reperfusion. RESULTS: CNH increased myocardial TNF- level and expression of TNFR2; this response was abolished by infliximab treatment. CNH reduced myocardial infarct size from 50.8 ± 4.3% of the area at risk in normoxic animals to 35.5 ± 2.4%. Infliximab abolished the protective effect of CNH (44.9 ± 2.0%). CNH increased the levels of oxidative stress markers (3-nitrotyrosine and malondialdehyde), the expression of nuclear factor κB and manganese superoxide dismutase, while these effects were absent in infliximab-treated animals. CNH-elevated levels of inducible nitric oxide synthase and cyclooxygenase 2 were not affected by infliximab. CONCLUSION: TNF- plays a role in the induction of ischaemia-resistant cardiac phenotype of CNH rats, possibly via the activation of protective redox signalling. |
| File Format | HTM / HTML |
| ISSN | 17481708 |
| Issue Number | 1 |
| Volume Number | 214 |
| e-ISSN | 17481716 |
| Journal | Acta Physiologica |
| Language | English |
| Publisher | Wiley-Blackwell |
| Publisher Date | 2015-05-01 |
| Publisher Place | Great Britain (UK) |
| Access Restriction | One Nation One Subscription (ONOS) |
| Subject Keyword | Discipline Physiology Adaptation, Physiological Physiology Anoxia Metabolism Myocardial Ischemia Myocardium Tumor Necrosis Factor-alpha Animals Heart Drug Effects Infliximab Pharmacology Male Nf-kappa B Nitric Oxide Synthase Type Ii Oxidative Stress Rats Rats, Wistar Receptors, Tumor Necrosis Factor, Type Ii Superoxide Dismutase Antagonists & Inhibitors Journal Article Research Support, Non-u.s. Gov't |
| Content Type | Text |
| Resource Type | Article |
| Subject | Physiology |
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