Počet záznamů: 1  

Excess ischemic tachyarrhythmias trigger protection infarction in rats

  1. 1.
    SYSNO ASEP0546478
    Druh ASEPJ - Článek v odborném periodiku
    Zařazení RIVJ - Článek v odborném periodiku
    Poddruh JČlánek ve WOS
    NázevExcess ischemic tachyarrhythmias trigger protection infarction in rats
    Tvůrce(i) Neckář, Jan (FGU-C) RID, ORCID
    Alánová, Petra (FGU-C) RID, ORCID
    Olejníčková, Veronika (FGU-C) RID, ORCID, SAI
    Papoušek, František (FGU-C)
    Hejnová, L. (CZ)
    Šilhavý, Jan (FGU-C) RID, ORCID
    Behuliak, Michal (FGU-C) RID, ORCID
    Bencze, Michal (FGU-C) RID, ORCID, SAI
    Hrdlička, Jaroslav (FGU-C) ORCID
    Vecka, M. (CZ)
    Jarkovská, D. (CZ)
    Švíglerová, J. (CZ)
    Mistrová, E. (CZ)
    Štengl, M. (CZ)
    Novotný, J. (CZ)
    Ošťádal, Bohuslav (FGU-C) RID
    Pravenec, Michal (FGU-C) RID, ORCID
    Kolář, František (FGU-C) RID, ORCID, SAI
    Zdroj.dok.Clinical science - ISSN 0143-5221
    Roč. 135, č. 17 (2021), s. 2143-2163
    Poč.str.21 s.
    Jazyk dok.eng - angličtina
    Země vyd.GB - Velká Británie
    Klíč. slovaC-reactive protein ; heart ; metabolomics ; myocardial infarction ; remote ischemic perconditioning ; ventricular arrhythmias
    Vědní obor RIVED - Fyziologie
    Obor OECDPhysiology (including cytology)
    CEPGA18-03207S GA ČR - Grantová agentura ČR
    Způsob publikováníOmezený přístup
    Institucionální podporaFGU-C - RVO:67985823
    UT WOS000702536100001
    EID SCOPUS85116954913
    DOI10.1042/CS20210648
    AnotaceIncreased level of C-reactive protein (CRP) is a risk factor for cardiovascular diseases, including myocardial infarction and hypertension. Here, we analyzed the effects of CRP overexpression on cardiac susceptibility to ischemia/reperfusion (I/R) injury in adult spontaneously hypertensive rats (SHR) expressing human CRP transgene (SHR-CRP). Using an in vivo model of coronary artery occlusion, we found that transgenic expression of CRP predisposed SHR-CRP to repeated and prolonged ventricular tachyarrhythmias. Excessive ischemic arrhythmias in SHR-CRP led to a significant reduction in infarct size (IS) compared with SHR. The proarrhythmic phenotype in SHR-CRP was associated with altered heart and plasma eicosanoids, myocardial composition of fatty acids (FAs) in phospholipids, and autonomic nervous system imbalance before ischemia. To explain unexpected IS-limiting effect in SHR-CRP, we performed metabolomic analysis of plasma before and after ischemia. We also determined cardiac ischemic tolerance in hearts subjected to remote ischemic perconditioning (RIPer) and in hearts ex vivo. Acute ischemia in SHR-CRP markedly increased plasma levels of multiple potent cardioprotective molecules that could reduce IS at reperfusion. RIPer provided IS-limiting effect in SHR that was comparable with myocardial infarction observed in naïve SHR-CRP. In hearts ex vivo, IS did not differ between the strains, suggesting that extra-cardiac factors play a crucial role in protection. Our study shows that transgenic expression of human CRP predisposes SHR-CRP to excess ischemic ventricular tachyarrhythmias associated with a drop of pump function that triggers myocardial salvage against lethal I/R injury likely mediated by protective substances released to blood from hypoxic organs and tissue at reperfusion.
    PracovištěFyziologický ústav
    KontaktLucie Trajhanová, lucie.trajhanova@fgu.cas.cz, Tel.: 241 062 400
    Rok sběru2022
    Elektronická adresahttps://doi.org/10.1042/CS20210648
Počet záznamů: 1