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Please use this identifier to cite or link to this item: http://hdl.handle.net/20.500.12710/19591
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dc.contributor.authorCobet, V.-
dc.contributor.authorPopovici, M.-
dc.contributor.authorCiobanu, L.-
dc.contributor.authorTacu, L.-
dc.contributor.authorIvanov, V.-
dc.contributor.authorPopovici, I.-
dc.contributor.authorMoraru, I.-
dc.contributor.authorCobet, E.-
dc.contributor.authorIvanov, M.-
dc.contributor.authorPanfile, E.-
dc.contributor.authorRotaru, V.-
dc.date.accessioned2022-01-20T13:12:29Z-
dc.date.available2022-01-20T13:12:29Z-
dc.date.issued2017-
dc.identifier.issn1879-0844-
dc.identifier.urihttps://onlinelibrary.wiley.com/doi/epdf/10.1002/ejhf.833-
dc.identifier.urihttp://repository.usmf.md/handle/20.500.12710/19591-
dc.description.abstractBackground:Inflammation is appreciated as a leading factor regarding car-diovascular disorders triggering and exacerbation. Nevertheless a promisingantinflammatory treatment concerning cardiac mismatch improvement is not yetconsolidated.Aim:The in vitro evaluation of cardiac effects of the TNF-alpha antagonist adminis-tration during diabetes-induced heart failure (DHF).Material and methods:DHF was classically reproduced in rats by i/p adminis-tration of streprozotocin (50 mg/kg, 5 days) – series 1 (of reference). TNF-alphaantagonist, TNF-McAb (TNF monoclonal antibody, analog of infliximab) has beenadministered i/p during DHF modeling and 5 days after – series 2. After 10 daysanimals of both series have been euthanized, and isolated heart was perfused inisovolumic regimen (Langendorff model) or exterior working (Neely-Rovetto model).Cardiac reactivity was assayed in: (1) hemodynamic effort due to pre- and afterload increase; (2) neuroendocrine activation modulated by action in diverse concentra-tions of norepinephrine, angiotensin II and endothelin-1 (ET-1); (3) in ischemia (30min) followed by reperfusion (45 min) syndrome.Results:TNF-alpha inhibition led to significant increase of cardiac output (CO) ineffort with volume and resistance respectively by 23,7 and 26,2% comparativelyto reference indices. Systolic pressure of left ventricle (LV) was in series 1 higher inall induced hemodynamic stress levels, but on aortic pressure of 100 and 120 cmH20 the increment was significant and averagely represented 18-19%. DHF wascharacterized by LV lusitropic function impairment, whose principal parameters,telediastolic pressure (LVTDP) and index of diastolic myocardial rigidity significantlydecreased during TNF-alpha inhibition by 26-28%. The norepinephrine action ledin DHF to inotrop-chronotropic effect dissociation, but endothelin-1 (ET-1) induceda negative inotropic effect, associated by CO reducing by 10,3%. TNF-alpha inhibi-tion led to appearance of positive inotropic effect to ET-1 action and cardiac outputincrease by 11%. Myocardial ischemic contracture assayed after 30 min of ischemiathereby of LVTDP is doubly more in DHF vs control pattern (56,3±3,6 vs 28,4±1,9mm Hg) and remains above on 45th min of reperfusion (39,2±2,5 vs 18,8±1,2mm Hg). TNF-McAb notably attenuated consequences of ischemia-reperfusionsyndrome, leading to LVTDP drop by 29,3% at finish of ischemia and by 26,8% atfinish of reperfusion.Conclusions:1. TNF-alpha inhibition during diabetes-induced heart failureimproved cardiac functionality, confirming the pathogenical role of inflamma-tion and, on the other hand, the therapeutic relevance of TNF-McAb regardingoutworn heart functioning in hemodynamic and neuroendocrine efforts.2. Most conspicuous TNF-McAb benefit has referred to appearance of positiveinotropic effect to ET-1 action and significant decrease of LV telediastolic pressureby around 29% in ischemia-reperfusion syndrome.en_US
dc.language.isoenen_US
dc.publisherEuropean Society of Cardiologyen_US
dc.relation.ispartofEuropean Journal of Heart Failure Special Issue: Abstracts of the Heart Failure 2017 and the 4th World Congress on Acute Heart Failure, Paris, France, 29 April – 2 May 2017en_US
dc.titleInflammation inhibition effects in diabetes induced heart failureen_US
dc.typeOtheren_US
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