-
Something wrong with this record ?
Heart remodelling affects ECG in rat DOCA/salt model
M. Laska, J. Vitous, R. Jirik, M. Hendrych, E. Drazanova, L. Kratka, J. Nadenicek, M. Novakova, T. Stracina
Status minimal Language English Country Czech Republic
Document type Journal Article
NLK
Directory of Open Access Journals
from 1991
Free Medical Journals
from 1998
PubMed Central
from 2020
ProQuest Central
from 2005-01-01
Medline Complete (EBSCOhost)
from 2006-01-01
Nursing & Allied Health Database (ProQuest)
from 2005-01-01
Health & Medicine (ProQuest)
from 2005-01-01
ROAD: Directory of Open Access Scholarly Resources
from 1998
- MeSH
- Desoxycorticosterone Acetate * MeSH
- Electrocardiography * MeSH
- Fibrosis MeSH
- Rats MeSH
- Sodium Chloride, Dietary adverse effects MeSH
- Disease Models, Animal MeSH
- Myocardium pathology MeSH
- Rats, Sprague-Dawley * MeSH
- Ventricular Remodeling * MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
Myocardial remodelling involves structural and functional changes in the heart, potentially leading to heart failure. The deoxycorticosterone acetate (DOCA)/salt model is a widely used experimental approach to study hypertension-induced cardiac remodelling. It allows to investigate the mechanisms underlying myocardial fibrosis and hypertrophy, which are key contributors to impaired cardiac function. In this study, myocardial remodelling in rat deoxycorticosterone acetate/salt model was examined over a three-week period. The experiment involved 11 male Sprague-Dawley rats, divided into two groups: fibrosis (n=6) and control (n=5). Myocardial remodelling was induced in the fibrosis group through unilateral nephrectomy, deoxyco-rticosterone acetate administration, and increased salt intake. The results revealed significant structural changes, including increased left ventricular wall thickness, myocardial fractional volume, and development of myocardial fibrosis. Despite these changes, left ventricular ejection fraction was preserved and even increased. ECG analysis showed significant prolongation of the PR interval and widening of the QRS complex in the fibrosis group, indicating disrupted atrioventricular and ventricular conduction, likely due to fibrosis and hypertrophy. Correlation analysis suggested a potential relationship between QRS duration and myocardial hypertrophy, although no significant correlations were found among other ECG parameters and structural changes detected by MRI. The study highlights the advantage of the DOCA/salt model in exploring the impact of myocardial remodelling on electrophysiological properties. Notably, this study is among the first to show that early myocardial remodelling in this model is accompanied by distinct electrophysiological changes, suggesting that advanced methods combined with established animal models can open new opportunities for research in this field. Key words Myocardial fibrosis, Remodelling, Animal model, DOCA-salt, Magnetic resonance imaging.
References provided by Crossref.org
- 000
- 00000naa a2200000 a 4500
- 001
- bmc25005538
- 003
- CZ-PrNML
- 005
- 20250312151244.0
- 007
- ta
- 008
- 250213s2024 xr f 000 0|eng||
- 009
- AR
- 024 7_
- $a 10.33549/physiolres.935512 $2 doi
- 035 __
- $a (PubMed)39808174
- 040 __
- $a ABA008 $b cze $d ABA008 $e AACR2
- 041 0_
- $a eng
- 044 __
- $a xr
- 100 1_
- $a Laska, M $u Department of Physiology, Faculty of Medicine, Masaryk University, Brno, Czech Republic. stracina@med.muni.cz
- 245 10
- $a Heart remodelling affects ECG in rat DOCA/salt model / $c M. Laska, J. Vitous, R. Jirik, M. Hendrych, E. Drazanova, L. Kratka, J. Nadenicek, M. Novakova, T. Stracina
- 520 9_
- $a Myocardial remodelling involves structural and functional changes in the heart, potentially leading to heart failure. The deoxycorticosterone acetate (DOCA)/salt model is a widely used experimental approach to study hypertension-induced cardiac remodelling. It allows to investigate the mechanisms underlying myocardial fibrosis and hypertrophy, which are key contributors to impaired cardiac function. In this study, myocardial remodelling in rat deoxycorticosterone acetate/salt model was examined over a three-week period. The experiment involved 11 male Sprague-Dawley rats, divided into two groups: fibrosis (n=6) and control (n=5). Myocardial remodelling was induced in the fibrosis group through unilateral nephrectomy, deoxyco-rticosterone acetate administration, and increased salt intake. The results revealed significant structural changes, including increased left ventricular wall thickness, myocardial fractional volume, and development of myocardial fibrosis. Despite these changes, left ventricular ejection fraction was preserved and even increased. ECG analysis showed significant prolongation of the PR interval and widening of the QRS complex in the fibrosis group, indicating disrupted atrioventricular and ventricular conduction, likely due to fibrosis and hypertrophy. Correlation analysis suggested a potential relationship between QRS duration and myocardial hypertrophy, although no significant correlations were found among other ECG parameters and structural changes detected by MRI. The study highlights the advantage of the DOCA/salt model in exploring the impact of myocardial remodelling on electrophysiological properties. Notably, this study is among the first to show that early myocardial remodelling in this model is accompanied by distinct electrophysiological changes, suggesting that advanced methods combined with established animal models can open new opportunities for research in this field. Key words Myocardial fibrosis, Remodelling, Animal model, DOCA-salt, Magnetic resonance imaging.
- 650 _2
- $a zvířata $7 D000818
- 650 _2
- $a mužské pohlaví $7 D008297
- 650 12
- $a remodelace komor $7 D020257
- 650 12
- $a potkani Sprague-Dawley $7 D017207
- 650 _2
- $a krysa rodu Rattus $7 D051381
- 650 12
- $a deoxykortikosteron-21-acetát $7 D064791
- 650 12
- $a elektrokardiografie $7 D004562
- 650 _2
- $a modely nemocí na zvířatech $7 D004195
- 650 _2
- $a kuchyňská sůl $x škodlivé účinky $7 D017673
- 650 _2
- $a fibróza $7 D005355
- 650 _2
- $a myokard $x patologie $7 D009206
- 655 _2
- $a časopisecké články $7 D016428
- 700 1_
- $a Vitous, J
- 700 1_
- $a Jirik, R
- 700 1_
- $a Hendrych, M
- 700 1_
- $a Drazanova, E
- 700 1_
- $a Kratka, L
- 700 1_
- $a Nadenicek, J
- 700 1_
- $a Novakova, M
- 700 1_
- $a Stracina, T
- 773 0_
- $w MED00003824 $t Physiological research $x 1802-9973 $g Roč. 73, Suppl. 3 (2024), s. S727-S753
- 856 41
- $u https://pubmed.ncbi.nlm.nih.gov/39808174 $y Pubmed
- 910 __
- $a ABA008 $b A 4120 $c 266 $y - $z 0
- 990 __
- $a 20250213 $b ABA008
- 991 __
- $a 20250312151250 $b ABA008
- 999 __
- $a min $b bmc $g 2283573 $s 1242558
- BAS __
- $a 3
- BAS __
- $a PreBMC-MEDLINE
- BMC __
- $a 2024 $b 73 $c Suppl. 3 $d S727-S753 $e 20241231 $i 1802-9973 $m Physiological research $n Physiol Res $x MED00003824
- LZP __
- $a Pubmed-20250213