Arrhythmogenesis in the Developing Heart During Anoxia‐Reoxygenation and Hypothermia‐Rewarming: An In Vitro Model

Sarre, Alexandre; Kučera, Pavel; Kappenberger, L; Raddatz, Eric

doi:10.1111/j.1540-8167.2006.00637.x

Cited by 26 publications

(44 citation statements)

References 49 publications

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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 Amentioning

confidence: 99%

“…Although the embryonic/fetal heart develops and functions normally in an intrauterine environment characterized by a low oxygen level, it reacts rapidly to abrupt oxygen shortage and reoxygenation (19,31,36,44). Such a stress was used in the context of ADO signaling to reveal possible functional differences between N and H6 hearts, which are not detectable otherwise.…”

Section: Adenosine Was Cardioprotective During Anoxiareoxygenationmentioning

confidence: 99%

“…1A). Arrhythmias induced by anoxia-reoxygenation were characterized mostly according to the classical diagnosis used in clinical human practice and were considered as present if documented at least once in a given recording (44). The efficiency of the atrio- ventricular (AV) propagation was calculated as the ratio of the ventricular to the atrial electrical activity duration and was expressed as a percentage, 100% representing one to one AV conduction (46).…”

mentioning

confidence: 99%

“…To determine to what extent the response of N and H hearts to anoxiareoxygenation can be differently altered by ADO, spontaneously beating hearts were placed in the culture compartment of an airtight chamber maintained at 37.5°C. Electrocardiogram (ECG) and contractile activity were recorded as described elsewhere in detail (44). ECG of the ex vivo embryonic heart displayed characteristic P, QRS, and T components, which allowed to assess PP and PR intervals, QT duration, amplitude, and width of the QRS complex and T wave.…”

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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 Amentioning

confidence: 99%

Section: Adenosine Was Cardioprotective During Anoxiareoxygenationmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

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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“…On the other hand, however, we have to consider that regional differences in the wall motion of tubular embryonic hearts have previously been documented by several other researchers and, thus are not really new findings (Boucek et al, 1959;Castenholz and Flórez-Cossio, 1972;Steding and Seidl, 1990;Sarre et al, 2006;Vennemann et al, 2006). Furthermore, the presence of a leading kickstart region at the cardiac inflow must not necessarily mean that the tubular embryonic heart owns only a single segment of active myocardial contractions.…”

Section: Solid (Morphological) Dynamicsmentioning

confidence: 99%

How does the tubular embryonic heart work? Looking for the physical mechanism generating unidirectional blood flow in the valveless embryonic heart tube

Männer

Wessel

Yelbuz

2010

Developmental Dynamics

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The heart is the first organ to function in vertebrate embryos. The human heart, for example, starts beating around the 21st embryonic day. During the initial phase of its pumping action, the embryonic heart is seen as a pulsating blood vessel that is built up by (1) an inner endothelial tube lacking valves, (2) a middle layer of extracellular matrix, and (3) an outer myocardial tube. Despite the absence of valves, this tubular heart generates unidirectional blood flow. This fact poses the question how it works. Visual examination of the pulsating embryonic heart tube shows that its pumping action is characterized by traveling mechanical waves sweeping from its venous to its arterial end. These traveling waves were traditionally described as myocardial peristaltic waves. It has, therefore, been speculated that the tubular embryonic heart works as a technical peristaltic pump. Recent hemodynamic data from living embryos, however, have shown that the pumping function of the embryonic heart tube differs in several respects from that of a technical peristaltic pump. Some of these data suggest that embryonic heart tubes work as valveless ''Liebau pumps.'' In the present study, a review is given on the evolution of the two above-mentioned theories of early cardiac pumping mechanics. We discuss pros and cons for both of these theories. We show that the tubular embryonic heart works neither as a technical peristaltic pump nor as a classic Liebau pump. The question regarding how the embryonic heart tube works still awaits an answer.

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Atrioventricular conduction and arrhythmias at the initiation of beating in embryonic mouse hearts

Chen

Diego

Chang

et al. 2010

Developmental Dynamics

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To investigate cardiac physiology at the onset of heart beating in embryonic mouse hearts, we performed optical imaging of membrane potential (Vm) and/or intracellular calcium (Ca i ). Action potentials and Ca i transients were detected in~50% of mouse embryo hearts at E8.5, but in all hearts at E9.0, indicating that beating typically starts between E8-E9. Beating was eliminated by Ca channel blocker nifedipine and the I f blocker ZD7288, unaffected by tetrodotoxin and only mildly depressed by disabling sarcoplasmic (SR) and endoplasmic (ER) reticulum Ca cycling. From E8.5 to E10, conduction velocity increased from 0.2-1 mm/s to >5 mm/s in first ventricular and then atrial tissue, while remaining slow in other areas. Arrhythmias included atrioventricular reentry induced by adenosine. In summary, at the onset of beating, I f -dependent pacemaking drives both AP propagation and Ca i transient generation through activation of voltage-dependent Ca channels. Na channels and intracellular Ca cycling have minor roles. Developmental Dynamics 239:1941-1949,

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Arrhythmogenesis in the Developing Heart During Anoxia‐Reoxygenation and Hypothermia‐Rewarming: An In Vitro Model

Abstract: In the embryonic heart, arrhythmias mainly originated in the sinoatrial tissue and resembled those observed in the adult heart. Furthermore, oxygen readmission was by far more arrhythmogenic than rewarming and the chronotropic, dromotropic, and inotropic effects were fully reversible.

Cited by 26 publications

References 49 publications

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

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

How does the tubular embryonic heart work? Looking for the physical mechanism generating unidirectional blood flow in the valveless embryonic heart tube

Atrioventricular conduction and arrhythmias at the initiation of beating in embryonic mouse hearts

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