Arrhythmias in the developing heart

Sedmera, David; Kočková, Radka; Vostarek, Frantisek; Raddatz, Eric

doi:10.1111/apha.12418

Cited by 13 publications

(11 citation statements)

References 128 publications

(223 reference statements)

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“…Anoxia and reoxygenation transiently and significantly altered electromechanical parameters and induced several types of arrhythmias in both N and H hearts. The principal types of arrhythmias were transient atrial tachycardia (range 180 -300 beats/min) and bradycardia (range 110 -140 beats/min), atrial ectopy, second degree AV blocks (2:1 to 8:1), Wenckebach phenomenon (Mobitz type I), third degree AV blocks (ventricular escape beats), and intermittent cardioplegia as previously documented (44,45). Some of these arrhythmias are illustrated in Fig.…”

Section: Expression Of Genes Involved In Ado Signaling Was Strongly Asupporting

confidence: 54%

“…However, hypoxia-induced imbalance between O 2 supply and demand impacts gene expression, metabolism, growth, and function (13,17,20,21,33,45,48,50,53,56). Oxygen deprivation during critical periods of embryogenesis impairs heart development and function with hemodynamic disturbances resulting in fetal growth retardation and increasing the risk of cardiovascular disease in adulthood, the so-called "fetal programming" (8,12,26,38,47,57,59).…”

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confidence: 99%

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

Robin

Marcillac

Raddatz

2015

American Journal of Physiology-Regulatory, Integrative and Comp

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Robin E, Marcillac F, Raddatz E. A hypoxic episode during cardiogenesis downregulates the adenosinergic system and alters the myocardial anoxic tolerance. Am J Physiol Regul Integr Comp Physiol 308: R614 -R626, 2015. First published January 28, 2015 doi:10.1152/ajpregu.00423.2014.-To what extent hypoxia alters the adenosine (ADO) system and impacts on cardiac function during embryogenesis is not known. Ectonucleoside triphosphate diphosphohydrolase (CD39), ecto-5=-nucleotidase (CD73), adenosine kinase (AdK), adenosine deaminase (ADA), equilibrative (ENT1,3,4), and concentrative (CNT3) transporters and ADO receptors A 1, A2A, A2B, and A3 constitute the adenosinergic system. During the first 4 days of development chick embryos were exposed in ovo to normoxia followed or not followed by 6 h hypoxia. ADO and glycogen content and mRNA expression of the genes were determined in the atria, ventricle, and outflow tract of the normoxic (N) and hypoxic (H) hearts. Electrocardiogram and ventricular shortening of the N and H hearts were recorded ex vivo throughout anoxia/reoxygenation Ϯ ADO. Under basal conditions, CD39, CD73, ADK, ADA, ENT1,3,4, CNT3, and ADO receptors were differentially expressed in the atria, ventricle, and outflow tract. In H hearts ADO level doubled, glycogen decreased, and mRNA expression of all the investigated genes was downregulated by hypoxia, except for A 2A and A3 receptors. The most rapid and marked downregulation was found for ADA in atria. H hearts were arrhythmic and more vulnerable to anoxia-reoxygenation than N hearts. Despite downregulation of the genes, exposure of isolated hearts to ADO 1) preserved glycogen through activation of A1 receptor and Akt-GSK3␤-GS pathway, 2) prolonged activity and improved conduction under anoxia, and 3) restored QT interval in H hearts. Thus hypoxia-induced downregulation of the adenosinergic system can be regarded as a coping response, limiting the detrimental accumulation of ADO without interfering with ADO signaling.anoxia-reoxygenation; arrhythmias; glycogen metabolism; hypoxia; adenosine signaling LOW OXYGEN LEVEL is a prerequisite for normal embryonic and fetal growth including the cardiovascular system. However, hypoxia-induced imbalance between O 2 supply and demand impacts gene expression, metabolism, growth, and function (13,17,20,21,33,45,48,50,53,56). Oxygen deprivation during critical periods of embryogenesis impairs heart development and function with hemodynamic disturbances resulting in fetal growth retardation and increasing the risk of cardiovascular disease in adulthood, the so-called "fetal programming" (8,12,26,38,47,57,59). Maternal hypoxemia, reduction in umbilical blood flow, or placental insufficiency can rapidly lead to acute or chronic ischemia and/or hypoxia, which exacerbates ATP-derived adenosine (ADO) production. Since ADO represents an important regulator of the embryonic cardiovascular function (35), the present study focuses on the modulation of the adenosinergic system by hypoxia and its functional consequences in the d...

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Section: Expression Of Genes Involved In Ado Signaling Was Strongly Asupporting

confidence: 54%

mentioning

confidence: 99%

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

Robin

Marcillac

Raddatz

2015

American Journal of Physiology-Regulatory, Integrative and Comp

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“…(3) When the excitation was spreading from this ectopic place, the activation time of both atria was even more prolonged than in the rest of the CX40À/À. We hypothesize that this could be a consequence of the presence of a preferential pathway (Bachmann's bundle) of signal spreading from the SAN to the left atrium, as described in the chick embryos [28] as well as other species [29] including humans [30]. This preferential pathway does not seem to be fully utilized during the ectopic activation (Fig.…”

Section: Discussionmentioning

confidence: 90%

The role of connexin40 in developing atrial conduction

et al. 2014

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a b s t r a c tConnexin40 (Cx40) is the main connexin expressed in the murine atria and ventricular conduction system. We assess here the developmental role of Cx40 in atrial conduction of the mouse. Cx40 deficiency significantly prolonged activation times in embryonic day 10.5, 12.5 and 14.5 atria during spontaneous activation; the severity decreased with increasing age. In a majority of Cx40 deficient mice the impulse originated from an ectopic focus in the right atrial appendage; in such a case the activation time was even longer due to prolonged activation. Cx40 has thus an important physiological role in the developing atria.

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“…Autonomic rhythm‐generating cells as, for example, in the heart (Sedmera et al . )? Rhythmic exercise (Hansen )?…”

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confidence: 99%

“…When a physiologist thinks "rhythm", what comes to his/her mind? Autonomic rhythm-generating cells as, for example, in the heart (Sedmera et al 2015)? Rhythmic exercise (Hansen 2015)?…”

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confidence: 99%