Melatonin reduces cardiac remodeling and improves survival in rats with isoproterenol-induced heart failure

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11150%2F14%3A10271859" target="_blank" >RIV/00216208:11150/14:10271859 - isvavai.cz</a>

Výsledek na webu

<a href="http://onlinelibrary.wiley.com/doi/10.1111/jpi.12154/pdf" target="_blank" >http://onlinelibrary.wiley.com/doi/10.1111/jpi.12154/pdf</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1111/jpi.12154" target="_blank" >10.1111/jpi.12154</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Melatonin reduces cardiac remodeling and improves survival in rats with isoproterenol-induced heart failure

Popis výsledku v původním jazyce

Melatonin was previously shown to reduce blood pressure and left ventricular remodeling in several models of experimental heart damage. Isoproterenol-induced heart failure with hypertrophy of the left and right ventricles, lowered systolic blood pressureand elevated pulmonary congestion. Fibrotic rebuilding was accompanied by alterations of tubulin level in the LV and oxidative stress development. Melatonin failed to reduce the weight of the LV or RV; however, it curtailed the weight of the lungs and attenuated the decline in SBP. Moreover, melatonin decreased the level of oxidative stress and insoluble and total collagen. Most importantly, melatonin reduced mortality and prolonged the average survival time. In conclusion, melatonin exerts cardioprotective effects and improves outcome in a model of isoproterenol-induced heart damage.

Název v anglickém jazyce

Melatonin reduces cardiac remodeling and improves survival in rats with isoproterenol-induced heart failure

Popis výsledku anglicky

Melatonin was previously shown to reduce blood pressure and left ventricular remodeling in several models of experimental heart damage. Isoproterenol-induced heart failure with hypertrophy of the left and right ventricles, lowered systolic blood pressureand elevated pulmonary congestion. Fibrotic rebuilding was accompanied by alterations of tubulin level in the LV and oxidative stress development. Melatonin failed to reduce the weight of the LV or RV; however, it curtailed the weight of the lungs and attenuated the decline in SBP. Moreover, melatonin decreased the level of oxidative stress and insoluble and total collagen. Most importantly, melatonin reduced mortality and prolonged the average survival time. In conclusion, melatonin exerts cardioprotective effects and improves outcome in a model of isoproterenol-induced heart damage.

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

ED - Fyziologie

OECD FORD obor

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Projekt

—

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2014

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Journal of Pineal Research

ISSN

0742-3098

e-ISSN

—

Svazek periodika

57

Číslo periodika v rámci svazku

2

Stát vydavatele periodika

DK - Dánské království

Počet stran výsledku

8

Strana od-do

177-184

Kód UT WoS článku

000342234000005

EID výsledku v databázi Scopus

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