Por favor, use este identificador para citar o enlazar este ítem:
http://hdl.handle.net/10201/71978
Twittear
Título: | Structural and functional alterations in the atrioventricular node and atrioventricular ring tissue in ischaemia-induced heart failure |
Fecha de publicación: | 2014 |
Editorial: | F. Hernández y Juan F. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología |
Cita bibliográfica: | Histology and Histopathology, Vol. 29, nº 7 (2014) |
ISSN: | 1699-5848 0213-3911 |
Materias relacionadas: | CDU::6 - Ciencias aplicadas::61 - Medicina |
Palabras clave: | Heart failure Atrioventricular node Atrioventricular ring |
Resumen: | Heart failure (HF) causes dysfunction of the atrioventricular node (AVN) – first or second-degree heart block is a risk factor for sudden cardiac death in HF patients. The aim of the study was to determine if HF causes remodelling of the AVN and right atrioventricular ring (RAVR). HF was induced in rats (n=4) by ligation of the proximal left coronary artery, which resulted in a large infarct of the left ventricle. Sham-operated rats (n=4) were used as controls. Eight weeks after surgery, functional experiments were performed and the hearts were frozen. The body weight of HF rats was similar to control rats, but the mean heart weight of HF rats was significantly enlarged. In HF rats compared to controls, the left ventricle was dilated, left ventricular enddiastolic pressure elevated (21.0±0.6 and 5.4±0.2 mm Hg), left ventricular ejection fraction reduced (0.2±0.02 and 0.5±0.02) and left ventricular end-systolic pressure reduced (102±4.2 and 127±3.1 mm Hg). In HF rats, the in vivo and in vitro PR intervals were increased (41% and 20%), as was the Wenckebach cycle length, indicative of AVN dysfunction. The collagen content was significantly increased in the AVN and RAVR indicating fibrosis. Immunolabelling of caveolin3 (cell membrane marker) showed that there was hypertrophy in HF (cell diameter was increased by 63%, 39% in AVN, RAVR). The TUNEL assay showed that the myocytes of the AVN and RAVR in HF undergo apoptotic cell death. Immunolabelling showed that expression of HCN4 was significantly decreased in the AVN and RAVR (43% and 47%) in HF. We conclude that in HF there is remodelling of the AVN and RAVR and this remodelling may explain the AVN dysfunction. |
Autor/es principal/es: | Yanni, Joseph Maczewski, MIchal Mackiewicz, Urszula Siew, Samuel Fedorenko, Olga Atkinson, Andrew Price, Marcus Beresewicz, Andrzej Anderson, Robert H. Boyett, Mark R. Dobrzynski, Halina |
URI: | http://hdl.handle.net/10201/71978 |
Tipo de documento: | info:eu-repo/semantics/article |
Número páginas / Extensión: | 12 |
Derechos: | info:eu-repo/semantics/openAccess Attribution-NonCommercial-NoDerivatives 4.0 International |
Aparece en las colecciones: | Vol.29, nº 7 (2014) |
Ficheros en este ítem:
Fichero | Descripción | Tamaño | Formato | |
---|---|---|---|---|
Yanni-29-891-902-2014.pdf | 39,52 MB | Adobe PDF | Visualizar/Abrir |
Este ítem está sujeto a una licencia Creative Commons Licencia Creative Commons