Developmental changes in cardiac recovery from anoxia-reoxygenation.
Détails
ID Serval
serval:BIB_C82D704F73D7
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Developmental changes in cardiac recovery from anoxia-reoxygenation.
Périodique
American Journal of Physiology. Regulatory, Integrative and Comparative Physiology
ISSN
0363-6119 (Print)
ISSN-L
0363-6119
Statut éditorial
Publié
Date de publication
2002
Peer-reviewed
Oui
Volume
283
Numéro
2
Pages
R379-R388
Langue
anglais
Résumé
The developing cardiovascular system is known to operate normally in a hypoxic environment. However, the functional and ultrastructural recovery of embryonic/fetal hearts subjected to anoxia lasting as long as hypoxia/ischemia performed in adult animal models remains to be investigated. Isolated spontaneously beating hearts from Hamburger-Hamilton developmental stages 14 (14HH), 20HH, 24HH, and 27HH chick embryos were subjected in vitro to 30 or 60 min of anoxia followed by 60 min of reoxygenation. Morphological alterations and apoptosis were assessed histologically and by transmission electron microscopy. Anoxia provoked an initial tachycardia followed by bradycardia leading to complete cardiac arrest, except for in the youngest heart, which kept beating. Complete atrioventricular block appeared after 9.4 +/- 1.1, 1.7 +/- 0.2, and 1.6 +/- 0.3 min at stages 20HH, 24HH, and 27HH, respectively. At reoxygenation, sinoatrial activity resumed first in the form of irregular bursts, and one-to-one atrioventricular conduction resumed after 8, 17, and 35 min at stages 20HH, 24HH, and 27HH, respectively. Ventricular shortening recovered within 30 min except at stage 27HH. After 60 min of anoxia, stage 27HH hearts did not retrieve their baseline activity. Whatever the stage and anoxia duration, nuclear and mitochondrial swelling observed at the end of anoxia were reversible with no apoptosis. Thus the embryonic heart is able to fully recover from anoxia/reoxygenation although its anoxic tolerance declines with age. Changes in cellular homeostatic mechanisms rather than in energy metabolism may account for these developmental variations.
Mots-clé
Animals, Anoxia/physiopathology, Bradycardia/physiopathology, Chick Embryo, Extracellular Space/chemistry, Extracellular Space/metabolism, Heart/drug effects, Heart/embryology, Heart Block/physiopathology, Heart Rate/drug effects, Hydrogen-Ion Concentration, Lactic Acid/biosynthesis, Oxygen/pharmacology, Recovery of Function, Tachycardia/physiopathology, Time Factors
Pubmed
Web of science
Création de la notice
24/01/2008 13:19
Dernière modification de la notice
20/08/2019 15:43