title: Myocardial enlargement in defective heart development.
abstract: BACKGROUND
  The cardiac neural crest (neural crest extending from the mid-otic placode to the caudal region of somite 3) provides ectomesenchymal cells that contribute to aortic arch development and are essential for aortico-pulmonary septation of the outflow tract. Bilateral ablation of the cardiac neural crest in the chick embryo, prior to migration, leads to aortic arch anomalies and failure of septation of the cardiac outflow tract, which produces a severe defect known as persistent truncus arteriosus (PTA). Altered hemodynamics resulting from abnormal aortic arch artery development and PTA and other unknown factors related to the absence of neural crest, are likely to alter the developmental history of the myocardium.
  
  
  METHODS
  In this study the wet and dry weights of ventricles and whole embryos, the total number of myocytes per ventricle and the myocyte density (number of myocytes per unit volume of ventricular myocardium) were compared in control (unwindowed eggs), sham-operated and cardiac neural crest ablated chick embryos at day 11 of incubation.
  
  
  RESULTS
  We found that the wet and dry weights of ventricles from hearts with PTA were not different from normal hearts in control and sham-operated embryos. However, the embryos with PTA weighed less than embryos with normal hearts. Thus, the ventricle to embryo weight ratios were greater in embryos with PTA compared to control and sham-operated embryos for both wet (14 and 20%, respectively) and dry (30 and 59%) weights. The data further implied that more water was present with respect to body weight in comparison with sham-operated and control embryos which indicated that the embryos with PTA were edematous. The total number of myocytes and the number of myocytes per unit volume were not different when comparing sham-operated with PTA. Further, there was no indication that the myocardium from hearts with PTA was abnormal despite the small size and edema of the embryos.
  
  
  CONCLUSIONS
  It appears that hemodynamic stresses, resulting from the structural defects produced by neural crest ablation, are insufficient to increase heart growth, although cardiac function is depressed as evidenced by edema and failure of the embryo to thrive.
authors.affiliation: Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta 30912-2000.
authors.forename: T L
authors.initials: TL
authors.lastname: Creazzo
authors.forename: J
authors.initials: J
authors.lastname: Burch
authors.forename: S
authors.initials: S
authors.lastname: Redmond
authors.forename: D
authors.initials: D
authors.lastname: Kumiski
mesh_terms: D000818:Animals; D006332:Cardiomegaly / Q000196:embryology*; D002452:Cell Count; D002642:Chick Embryo; D005314:Embryonic and Fetal Development; D006321:Heart / Q000196:embryology*; D006352:Heart Ventricles