Physiopathology of the embryonic heart (with special emphasis on hypoxia and reoxygenation)

Physiopathology of the embryonic heart (with special emphasis on hypoxia and reoxygenation)
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DOI:
10.1016/j.ancard.2006.02.007
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发表时间:
2006-04-01
期刊:
Annales de Cardiologie et d'Angeiologie
影响因子:
--
通讯作者:
Sarre, A.
Sarre, A.
中科院分区:
其他
文献类型:
--
作者:
Raddatz, E.;Gardier, S.;Sarre, A.

文献摘要

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发育中的心脏对不利的宫内环境的适应性反应,如减少O-2输送,可导致基因表达的改变,具有短期和长期的后果,包括成人心血管疾病。发育中的心脏对急性或慢性缺氧的耐受性、再灌注期间的恢复能力以及复氧损伤的机制仍存在争议。事实上,未成熟心肌对缺氧-复氧的反应模式与成人不同。本文综述了胚胎心脏的结构和代谢特征以及缺氧和复氧的功能后果。检查钙和钠过载、pH紊乱和氧化应激对缺氧诱导的心功能障碍的相对贡献,以及涉及细胞存活或死亡的各种细胞信号传导途径(例如MAP激酶)。在发育心脏病学和胎儿心脏手术的最新进展的背景下,需要更好地了解应激发育心脏的生理病理学。(c)2006年爱思唯尔SAS。All rights reserved.
The adaptative response of the developing heart to adverse intrauterine environment such as reduced O-2 delivery can result in alteration of gene expression with short- and long-term consequences including adult cardiovascular diseases. The tolerance of the developing heart of acute or chronic oxygen deprivation, its capacity to recover during reperfusion and the mechanisms involved in reoxygenation injury are still under debate. Indeed, the pattern of response of the immature myocardium to hypoxia-reoxygenation differs from that of the adult. This review deals with the structural and metabolic characteristics of the embryonic heart and the functional consequences of hypoxia and reoxygenation. The relative contribution of calcium and sodium overload, pH disturbances and oxidant stress to the hypoxia-induced cardiac dysfunction is examined, as well as various cellular signaling pathways (e.g. MAP kinases) involved in cell survival or death. In the context of the recent advances in developmental cardiology and fetal cardiac surgery, a better understanding of the physiopathology of the stressed developing heart is required. (c) 2006 Elsevier SAS. All rights reserved.