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
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Czech description
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Classification
Type
J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database
CEP classification
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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