Literature DB >> 11228262

Oxidative and glycogenolytic cCapacities within the developing chick heart.

R Romano1, A C Rochat, P Kucera, Y De Ribaupierre, E Raddatz.   

Abstract

Cardiac morphogenesis and function are known to depend on both aerobic and anaerobic energy-producing pathways. However, the relative contribution of mitochondrial oxidation and glycogenolysis, as well as the determining factors of oxygen demand in the distinct chambers of the embryonic heart, remains to be investigated. Spontaneously beating hearts isolated from stage 11, 20, and 24HH chick embryos were maintained in vitro under controlled metabolic conditions. O(2) uptake and glycogenolytic rate were determined in atrium, ventricle, and conotruncus in the absence or presence of glucose. Oxidative capacity ranged from 0.2 to 0.5 nmol O(2)/(h.microg protein), did not depend on exogenous glucose, and was the highest in atria at stage 20HH. However, the highest reserves of oxidative capacity, assessed by mitochondrial uncoupling, were found at the youngest stage and in conotruncus, representing 75 to 130% of the control values. At stage 24HH, glycogenolysis in glucose-free medium was 0.22, 0.17, and 0.04 nmol glucose U(h.microg protein) in atrium, ventricle, and conotruncus, respectively. Mechanical loading of the ventricle increased its oxidative capacity by 62% without altering glycogenolysis or lactate production. Blockade of glycolysis by iodoacetate suppressed lactate production but modified neither O(2) nor glycogen consumption in substrate-free medium. These findings indicate that atrium is the cardiac chamber that best utilizes its oxidative and glycogenolytic capacities and that ventricular wall stretch represents an early and major determinant of the O(2) uptake. Moreover, the fact that O(2) and glycogen consumptions were not affected by inhibition of glyceraldehyde-3-phosphate dehydrogenase provides indirect evidence for an active glycerol-phosphate shuttle in the embryonic cardiomyocytes.

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Year:  2001        PMID: 11228262     DOI: 10.1203/00006450-200103000-00010

Source DB:  PubMed          Journal:  Pediatr Res        ISSN: 0031-3998            Impact factor:   3.756


  5 in total

1.  Transient anoxia and oxyradicals induce a region-specific activation of MAPKs in the embryonic heart.

Authors:  Stephany Gardier; Sarah Pedretti; Alexandre Sarre; Eric Raddatz
Journal:  Mol Cell Biochem       Date:  2010-03-21       Impact factor: 3.396

2.  Modulation of the c-Jun N-terminal kinase activity in the embryonic heart in response to anoxia-reoxygenation: involvement of the Ca2+ and mitoKATP channels.

Authors:  Alexandre Sarre; Stéphany Gardier; Fabienne Maurer; Christophe Bonny; Eric Raddatz
Journal:  Mol Cell Biochem       Date:  2008-04-17       Impact factor: 3.396

3.  A hypoxic episode during cardiogenesis downregulates the adenosinergic system and alters the myocardial anoxic tolerance.

Authors:  Elodie Robin; Fabrice Marcillac; Eric Raddatz
Journal:  Am J Physiol Regul Integr Comp Physiol       Date:  2015-01-28       Impact factor: 3.619

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

Authors:  J Terrand; E Felley-Bosco; F Courjault-Gautier; A C Rochat; P Kucera; E Raddatz
Journal:  Mol Cell Biochem       Date:  2003-10       Impact factor: 3.396

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

Authors:  Philippe Maury; Alexandre Sarre; Jérôme Terrand; Antonio Rosa; Pavel Kucera; Lukas Kappenberger; Eric Raddatz
Journal:  Mol Cell Biochem       Date:  2004-10       Impact factor: 3.396

  5 in total

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