The Journal of Thoracic and Cardiovascular Surgery
Volume 160, Issue 3, September 2020, Pages e135-e144
Adult: Coronary: Basic ScienceEffect of bilateral sympathectomy in a rat model of dilated cardiomyopathy induced by doxorubicin
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Graphical abstract
After a cardiac insult and myocardium overload, the sympathetic nervous system activity increases as a compensatory mechanism. However, this mechanism leads to further decompensation with ventricular remodeling observed by an enlarged left ventricle, myocardial extracellular fibrosis, increased apoptosis, and subsequent loss of function. With sympathetic blockade, LV remodeling was prevented and cardiac function was preserved.
Key Words
sympathectomy
dilated cardiomyopathy
doxorubicin
left ventricular remodeling
left ventricular function
apoptosis
Abbreviations and Acronyms
ACEI
angiotensin-converting enzyme inhibitor
BS
bilateral sympathectomy
DBT
dobutamine
DCM
dilated cardiomyopathy
HR
heart rate
ICAM
intercellular adhesion cellular molecule
LS
left sympathectomy
LV
left ventricular
LVEF
left ventricular ejection fraction
LVSW
left ventricular stroke work
MMP
matrix metalloproteinase
PRSW
preload recruitable stroke work
TBST
tris-buffered saline Tween-20
VEGF
vascular endothelial growth factor
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This study was financed in part by the Coordenação de Aperfeiçoamento de Pessoal de Nível Superior–Brasil (CAPES)–Finance Code 001.
© 2019 by The American Association for Thoracic Surgery