title: Bilateral sympathectomy improves postinfarction left ventricular remodeling and function.
abstract: To evaluate the influence of bilateral or left sympathectomy on left ventricular remodeling and function after myocardial infarction in rats.
  
  
  
  Myocardial infarction was induced in rats by ligation of the left anterior descending coronary. Seven days later, rats were divided into 4 groups: the myocardial infarction, myocardial infarction with left sympathectomy, myocardial infarction with bilateral sympathectomy, and sham groups. After 8 weeks, left ventricular function was evaluated with the use of a pressure-volume conductance catheter under steady-state conditions and pharmacological stress. Infarct size and extracellular matrix fibrosis were evaluated, and cardiac matrix metalloproteinases and myocardial inflammatory markers were analyzed.
  
  
  
  The myocardial infarction and left sympathectomy group had an increased end diastolic volume, whereas the bilateral sympathectomy group had a mean end-diastolic volume similar to that of the sham group (P < .002). Significant reduction in ejection fraction was observed in the myocardial infarction and left sympathectomy group, whereas it was preserved after bilateral sympathectomy (P < .001). In response to dobutamine, left ventricular contractility increased in sham rats, rising stroke work, cardiac output, systolic volume, end-diastolic volume, ejection fraction, and dP/dt max. Only bilateral sympathectomy rats had significant increases in ejection fraction (P < .001) with dobutamine. Fibrotic tissue and matrix metalloproteinase expression decreased in the bilateral sympathectomy group compared to that in the myocardial infarction group (P < .001) and was associated with left ventricular wall thickness maintenance and better apoptotic markers in noninfarcted myocardium.
  
  
  
  Bilateral sympathectomy effectively attenuated left ventricular remodeling and preserved systolic function after myocardial infarction induction in rats.
authors.affiliation: Laboratory of Cardiovascular Surgery and Pathophysiology of Circulation, Heart Institute (Incor), Department of Cardiopneumology, Sao Paulo University Medical School, Sao Paulo, Brazil. Electronic address: zanoni@usp.br.
authors.forename: Fernando Luiz
authors.initials: FL
authors.lastname: Zanoni
authors.affiliation: Laboratory of Cardiovascular Surgery and Pathophysiology of Circulation, Heart Institute (Incor), Department of Cardiopneumology, Sao Paulo University Medical School, Sao Paulo, Brazil.
authors.forename: Rafael
authors.initials: R
authors.lastname: Simas
authors.affiliation: Laboratory of Cardiovascular Surgery and Pathophysiology of Circulation, Heart Institute (Incor), Department of Cardiopneumology, Sao Paulo University Medical School, Sao Paulo, Brazil.
authors.forename: Raphael Grillo
authors.initials: RG
authors.lastname: da Silva
authors.affiliation: Laboratory of Cardiovascular Surgery and Pathophysiology of Circulation, Heart Institute (Incor), Department of Cardiopneumology, Sao Paulo University Medical School, Sao Paulo, Brazil.
authors.forename: Ana Cristina
authors.initials: AC
authors.lastname: Breithaupt-Faloppa
authors.affiliation: Laboratory of Cardiovascular Surgery and Pathophysiology of Circulation, Heart Institute (Incor), Department of Cardiopneumology, Sao Paulo University Medical School, Sao Paulo, Brazil.
authors.forename: Raphael Dos Santos
authors.initials: RD
authors.lastname: Coutinho E Silva
authors.affiliation: Laboratory of Cardiovascular Surgery and Pathophysiology of Circulation, Heart Institute (Incor), Department of Cardiopneumology, Sao Paulo University Medical School, Sao Paulo, Brazil.
authors.forename: Fábio Biscegli
authors.initials: FB
authors.lastname: Jatene
authors.affiliation: Laboratory of Cardiovascular Surgery and Pathophysiology of Circulation, Heart Institute (Incor), Department of Cardiopneumology, Sao Paulo University Medical School, Sao Paulo, Brazil.
authors.forename: Luiz Felipe P
authors.initials: LF
authors.lastname: Moreira
mesh_terms: D000818:Animals; D017209:Apoptosis; D002395:Catecholamines / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D005355:Fibrosis; D006352:Heart Ventricles / Q000294:innervation* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D008297:Male; D020778:Matrix Metalloproteinase 2 / Q000378:metabolism; D020780:Matrix Metalloproteinase 9 / Q000378:metabolism; D009200:Myocardial Contraction; D009203:Myocardial Infarction / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000601:surgery*; D020097:Natriuretic Peptide, Brain / Q000378:metabolism; D017208:Rats, Wistar; D020127:Recovery of Function; D013318:Stroke Volume; D013562:Sympathectomy / Q000379:methods*; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism; D016277:Ventricular Function, Left; D020257:Ventricular Remodeling
chemical_list: D002395:Catecholamines; D016207:Cytokines; D042461:Vascular Endothelial Growth Factor A; C467498:vascular endothelial growth factor A, rat; D020097:Natriuretic Peptide, Brain; D020778:Matrix Metalloproteinase 2; C522363:Mmp2 protein, rat; D020780:Matrix Metalloproteinase 9; C572337:Mmp9 protein, rat
keywords: extracellular matrix; sympathectomy; ventricular remodeling