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Excess ischemic tachyarrhythmias trigger protection infarction in rats

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985823%3A_____%2F21%3A00546478" target="_blank" >RIV/67985823:_____/21:00546478 - isvavai.cz</a>

  • Alternative codes found

    RIV/00023001:_____/21:00081717

  • Result on the web

    <a href="https://doi.org/10.1042/CS20210648" target="_blank" >https://doi.org/10.1042/CS20210648</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1042/CS20210648" target="_blank" >10.1042/CS20210648</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Excess ischemic tachyarrhythmias trigger protection infarction in rats

  • Original language description

    Increased 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.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    30105 - Physiology (including cytology)

Result continuities

  • Project

    <a href="/en/project/GA18-03207S" target="_blank" >GA18-03207S: Cardiac ischemic tolerance of spontaneously hypertensive rats expressing human C-reactive protein.</a><br>

  • Continuities

    P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Others

  • Publication year

    2021

  • Confidentiality

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

Data specific for result type

  • Name of the periodical

    Clinical science

  • ISSN

    0143-5221

  • e-ISSN

    1470-8736

  • Volume of the periodical

    135

  • Issue of the periodical within the volume

    17

  • Country of publishing house

    GB - UNITED KINGDOM

  • Number of pages

    21

  • Pages from-to

    2143-2163

  • UT code for WoS article

    000702536100001

  • EID of the result in the Scopus database

    2-s2.0-85116954913