Postanoxic functional recovery of the developing heart is slightly altered by endogenous or exogenous nitric oxide.

Détails

ID Serval
serval:BIB_B6E8A84E5F46
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Postanoxic functional recovery of the developing heart is slightly altered by endogenous or exogenous nitric oxide.
Périodique
Molecular and Cellular Biochemistry
Auteur(s)
Terrand J., Felley-Bosco E., Courjault-Gautier F., Rochat A.C., Kucera P., Raddatz E.
ISSN
0300-8177 (Print)
ISSN-L
0300-8177
Statut éditorial
Publié
Date de publication
2003
Peer-reviewed
Oui
Volume
252
Numéro
1-2
Pages
53-63
Langue
anglais
Notes
Publication types: Journal Article
Publication Status: ppublish
Résumé
Nitric oxide synthase (NOS) is strongly and transiently expressed in the developing heart but its function is not well documented. This work examined the role, either protective or detrimental, that endogenous and exogenous NO could play in the functioning of the embryonic heart submitted to hypoxia and reoxygenation. Spontaneously beating hearts isolated from 4-day-old chick embryos were either homogenized to determine basal inducible NOS (iNOS) expression and activity or submitted to 30 min anoxia followed by 100 min reoxygenation. The chrono-, dromo- and inotropic responses to anoxia/reoxygenation were determined in the presence of NOS substrate (L-arginine 10 mM), NOS inhibitor L-NIO (1-5 mM), or NO donor (DETA NONOate 10-100 microM). Myocardial iNOS was detectable by immunoblotting and its activity was specifically decreased by 53% in the presence of 5 mM L-NIO. L-Arginine, L-NIO and DETA NONOate at 10 microM had no significant effect on the investigated functional parameters during anoxia/reoxygenation. However, irrespective of anoxia/reoxygenation, DETA NONOate at 100 microM decreased ventricular shortening velocity by about 70%, and reduced atrio-ventricular propagation by 23%. None of the used drugs affected atrial activity and hearts of all experimental groups fully recovered at the end of reoxygenation. These findings indicate that (1) by contrast with adult heart, endogenously released NO plays a minor role in the early response of the embryonic heart to reoxygenation, (2) exogenous NO has to be provided at high concentration to delay postanoxic functional recovery, and (3) sinoatrial pacemaker cells are the less responsive to NO.
Mots-clé
Animals, Anoxia/physiopathology, Blotting, Western, Chick Embryo, Heart/drug effects, Heart/embryology, Myocardium/enzymology, Nitric Oxide/pharmacology, Nitric Oxide/physiology, Nitric Oxide Synthase/metabolism, Nitric Oxide Synthase Type II
Pubmed
Web of science
Création de la notice
24/01/2008 13:19
Dernière modification de la notice
20/08/2019 15:25
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