title: Ventricular but not atrial electro-mechanical delay of the embryonic heart is altered by anoxia-reoxygenation and improved by nitric oxide.
abstract: OBJECTIVE
  Excitation-contraction coupling is modulated by nitric oxide (NO) which otherwise has either beneficial or detrimental effects on myocardial function during hypoxia-reoxygenation. This work aimed at characterizing the variations of electromechanical delay (EMD) induced by anoxia-reoxygenation within the developing heart and determining whether atrial and ventricular EMD are modulated by NO to the same extent.
  
  
  METHODS
  Hearts of 4 or 4.5-day-old chick embryos were excised and submitted in vitro to normoxia (45 min), anoxia (30 min) and reoxygenation (60 min). Electrocardiogram and atrial and ventricular contractions were simultaneously recorded throughout experiment. Anoxia-reoxygenation-induced chrono-, dromo-and inotropic disturbances and changes in EMD in atrium (EMDa) and ventricle (EMDv) were investigated in control hearts and in hearts exposed to 0.1, 1, 10, 50 and 100 microM of DETA-NONOate (a NO donating agent) or to 50 microM of L-NAME (a NOS inhibitor).
  
  
  RESULTS
  Under normoxia, heart rate, PR interval, ventricular shortening velocity, EMDa and EMDv were similar in control, L-NAME-treated and DETA-NONOate-treated hearts. Under anoxia, cardiac activity became markedly erratic within less than 10 min in all groups. At the onset of reoxygenation, EMDv was increased by about 300% with respect to the preanoxic value while EMDa did not vary significatively. Compared to control conditions, L-NAME or DETA-NONOate had no influence on the negative chrono-, dromo- and inotropic effects induced by anoxia-reoxygenation. However, L-NAME prolonged EMDv during anoxia and delayed EMDv recovery during reoxygenation while 100 microM DETA-NONOate had the opposite effects. EMDa was neither affected by NOS inhibitor nor NO donor. At the end of reoxygenation, all the investigated parameters returned to their basal values.
  
  
  CONCLUSIONS
  This work provides evidence that a NO-dependent pathway is involved in regulation of the ventricular excitation-contraction coupling in the anoxic-reoxygenated developing heart.
authors.affiliation: Division of Cardiology, University Hospital, Lausanne, Switzerland.
authors.forename: Philippe
authors.initials: P
authors.lastname: Maury
authors.forename: Alexandre
authors.initials: A
authors.lastname: Sarre
authors.forename: Jérôme
authors.initials: J
authors.lastname: Terrand
authors.forename: Antonio
authors.initials: A
authors.lastname: Rosa
authors.forename: Pavel
authors.initials: P
authors.lastname: Kucera
authors.forename: Lukas
authors.initials: L
authors.lastname: Kappenberger
authors.forename: Eric
authors.initials: E
authors.lastname: Raddatz
mesh_terms: D000818:Animals; D002642:Chick Embryo; D002645:Chickens; D004562:Electrocardiography; D004594:Electrophysiology / Q000379:methods; D006321:Heart / Q000196:embryology*; D006325:Heart Atria / Q000196:embryology; D006352:Heart Ventricles / Q000196:embryology / Q000473:pathology*; D000860:Hypoxia / Q000378:metabolism; D066298:In Vitro Techniques; D009200:Myocardial Contraction; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000737:chemistry* / Q000378:metabolism; D009603:Nitroso Compounds / Q000494:pharmacology; D010100:Oxygen / Q000378:metabolism; D015427:Reperfusion Injury; D015398:Signal Transduction; D013997:Time Factors
chemical_list: D009603:Nitroso Compounds; C094210:2,2'-(hydroxynitrosohydrazono)bis-ethanamine; D009569:Nitric Oxide; D010100:Oxygen; D019331:NG-Nitroarginine Methyl Ester