Ventricular but not atrial electro-mechanical delay of the embryonic heart is altered by anoxia-reoxygenation and improved by nitric oxide.

Details

Serval ID
serval:BIB_8927D3DDFDB9
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Ventricular but not atrial electro-mechanical delay of the embryonic heart is altered by anoxia-reoxygenation and improved by nitric oxide.
Journal
Molecular and Cellular Biochemistry
Author(s)
Maury P., Sarre A., Terrand J., Rosa A., Kucera P., Kappenberger L., Raddatz E.
ISSN
0300-8177 (Print)
ISSN-L
0300-8177
Publication state
Published
Issued date
2004
Volume
265
Number
1-2
Pages
141-149
Language
english
Abstract
BACKGROUND/AIM: 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.
CONCLUSION: 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.
Keywords
Animals, Anoxia/metabolism, Chick Embryo, Chickens, Electrocardiography, Electrophysiology/methods, Heart/embryology, Heart Atria/embryology, Heart Ventricles/embryology, Heart Ventricles/pathology, Myocardial Contraction, Myocardium/metabolism, Myocardium/pathology, NG-Nitroarginine Methyl Ester/pharmacology, Nitric Oxide/chemistry, Nitric Oxide/metabolism, Nitroso Compounds/pharmacology, Oxygen/metabolism, Reperfusion Injury, Signal Transduction, Time Factors
Pubmed
Web of science
Create date
24/01/2008 13:19
Last modification date
20/08/2019 14:48
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