Inhibition of bicarbonate transport protects embryonic heart against reoxygenation-induced dysfunction.

Détails

ID Serval
serval:BIB_F436B9C7740B
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Inhibition of bicarbonate transport protects embryonic heart against reoxygenation-induced dysfunction.
Périodique
Journal of Molecular and Cellular Cardiology
Auteur(s)
Meiltz A., Kucera P., de Ribaupierre Y., Raddatz E.
ISSN
0022-2828 (Print)
ISSN-L
0022-2828
Statut éditorial
Publié
Date de publication
1998
Volume
30
Numéro
2
Pages
327-335
Langue
anglais
Résumé
It has not been well established whether the mechanisms participating in pH regulation in the anoxic-reoxygenated developing myocardium resemble those operating in the adult. We have specially examined the importance of Na+/H+ exchange (NHE) and HCO3-dependent transports in cardiac activity after changes in extracellular pH (pHo). Spontaneously contracting hearts isolated from 4-day-old chick embryos were submitted to single or repeated anoxia (1 min) followed by reoxygenation (10 min). The chronotropic, dromotropic and inotropic responses of the hearts were determined in standard HCO3- buffer at pHo 7.4 and at pHo 6.5 (hypercapnic acidosis). In distinct experiments, acidotic anoxia preceded reoxygenation at pHo 7.4. NHE was blocked with amiloride derivative HMA (1 micro mol/l) and HCO3-dependent transports were inactivated by replacement of HCO3 or blockade with stilbene derivative DIDS (100 micro mol/l). Anoxia caused transient tachycardia, depressed mechanical function and induced contracture. Reoxygenation temporarily provoked cardiac arrest, atrio-ventricular (AV) block, arrhythmias and depression of contractility. Addition of DIDS or substitution of HCO3 at pHo 7.4 had the same effects as acidosis per se, i.e. shortened contractile activity and increased incidence of arrhythmias during anoxia, prolonged cardioplegia and provoked arrhythmias at reoxygenation. Under anoxia at pHo 6.5/reoxygenation at pHo 7.4, cardioplegia, AV block and arrhythmias were all markedly prolonged. Interestingly, in the latter protocol, DIDS suppressed AV block and arrhythmias during reoxygenation, whereas HMA had no effect. Thus, intracellular pH regulation in the anoxic-reoxygenated embryonic heart appears to depend predominantly on HCO3 availability and transport. Furthermore, pharmacological inhibition of anion transport can protect against reoxygenation-induced dysfunction.
Mots-clé
4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid/pharmacology, Acidosis/metabolism, Acidosis/physiopathology, Amiloride/analogs & derivatives, Amiloride/pharmacology, Animals, Arrhythmias, Cardiac/metabolism, Arrhythmias, Cardiac/physiopathology, Bicarbonates/metabolism, Chick Embryo, Heart/drug effects, Heart Rate, Hydrogen-Ion Concentration, Ion Transport/drug effects, Myocardial Contraction, Myocardial Ischemia/metabolism, Myocardial Ischemia/physiopathology, Myocardial Reperfusion Injury/metabolism, Myocardial Reperfusion Injury/physiopathology, Myocardium/metabolism, Sodium-Hydrogen Antiporter/antagonists & inhibitors, Sodium-Hydrogen Antiporter/metabolism
Pubmed
Web of science
Création de la notice
24/01/2008 14:19
Dernière modification de la notice
03/03/2018 22:43
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