Tolerance of isolated rat hearts to low-flow ischemia and hypoxia of increasing duration: protective role of down-regulation and ATP during ischemia

Détails

ID Serval
serval:BIB_D67274737CB2
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Tolerance of isolated rat hearts to low-flow ischemia and hypoxia of increasing duration: protective role of down-regulation and ATP during ischemia
Périodique
Molecular and Cellular Biochemistry
Auteur(s)
Milano  G., Corno  A. F., de Jong  J. W., von Segesser  L. K., Samaja  M.
ISSN
0300-8177
Statut éditorial
Publié
Date de publication
10/2001
Peer-reviewed
Oui
Volume
226
Numéro
1-2
Pages
141-51
Notes
Journal Article
Research Support, Non-U.S. Gov't --- Old month value: Oct
Résumé
We tested the hypothesis that down-regulated hearts, as observed during low-flow ischemia, adapt better to low O2 supply than non-down-regulated, or hypoxic, hearts. To address the link between down-regulation and endogenous ischemic protection, we compared myocardial tolerance to ischemia and hypoxia of increasing duration. To that end, we exposed buffer-perfused rat hearts to either low-flow ischemia or hypoxia (same O2 shortage) for 20, 40 or 60 min (n = 8/group), followed by reperfusion or reoxygenation (20 min, full O2 supply). At the end of the O2 shortage, the rate-pressure product was less in ischemic than hypoxic hearts (p < 0.0001). The recovery of the rate-pressure product after reperfusion or reoxygenation was not different for t = 20 min, but was better in ischemic than hypoxic hearts for t = 40 and 60 min (p < 0.02 and p < 0.0002, respectively). The end-diastolic pressure remained unchanged during low-flow ischemia (0.024 +/- 0.013 mmHg x min(-1)), but increased significantly during hypoxia (0.334 +/- 0.079 mmHg x min(-1)). We conclude that, while the duration of hypoxia progressively impaired the rate-pressure product and the end-diastolic pressure, hearts were insensitive of the duration of low-flow ischemia, thereby providing evidence that myocardial down-regulation protects hearts from injury. Excessive ATP catabolism during ischemia in non-down-regulated hearts impaired myocardial recovery regardless of vascular, blood-related and neuro-hormonal factors. These observations support the view that protection is mediated by the maintenance of the ATP pool.
Mots-clé
Adenosine Triphosphate/*metabolism Animals *Anoxia *Down-Regulation Heart/physiology Hydrogen-Ion Concentration *Ischemia Male Myocardium/metabolism Oxygen/metabolism Rats Rats, Sprague-Dawley Time Factors
Pubmed
Web of science
Création de la notice
18/01/2008 14:38
Dernière modification de la notice
20/08/2019 15:56
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