Control of the heart rate of rat embryos during the organogenic period

H. Ritchie, Carolina Ragnerstam, Elin Gustafsson, Johanna M Jonsson, W. Webster
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引用次数: 3

Abstract

The aim of this study was to gain insight into whether the first trimester embryo could control its own heart rate (HR) in response to hypoxia. The gestational day 13 rat embryo is a good model for the human embryo at 5–6 weeks gestation, as the heart is comparable in development and, like the human embryo, has no functional autonomic nerve supply at this stage. Utilizing a whole-embryo culture technique, we examined the effects of different pharmacological agents on HR under normoxic (95% oxygen) and hypoxic (20% oxygen) conditions. Oxygen concentrations ≤60% caused a concentration-dependent decrease in HR from normal levels of ~210 bpm. An adenosine agonist, AMP-activated protein kinase (AMPK) activator and KATP channel opener all caused bradycardia in normoxic conditions; however, putative antagonists for these systems failed to prevent or ameliorate hypoxia-induced bradycardia. This suggests that the activation of one or more of these systems is not the primary cause of the observed hypoxia-induced bradycardia. Inhibition of oxidative phosphorylation also decreased HR in normoxic conditions, highlighting the importance of ATP levels. The β-blocker metoprolol caused a concentration-dependent reduction in HR supporting reports that β1-adrenergic receptors are present in the early rat embryonic heart. The cAMP inducer colforsin induced a positive chronotropic effect in both normoxic and hypoxic conditions. Overall, the embryonic HR at this stage of development is responsive to the level of oxygenation, probably as a consequence of its influence on ATP production.
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大鼠胚胎器官发生期心率的控制
这项研究的目的是深入了解妊娠早期胚胎是否可以控制自身的心率(HR)以应对缺氧。妊娠第13天的大鼠胚胎是妊娠5-6周的人类胚胎的良好模型,因为心脏在发育上与人类胚胎相当,并且与人类胚胎一样,在这一阶段没有功能性的自主神经供应。利用全胚培养技术,我们在常氧(95%氧气)和低氧(20%氧气)条件下检测了不同药物对HR的影响。氧浓度≤60%导致心率从正常水平~210 bpm的浓度依赖性下降。腺苷激动剂、amp活化蛋白激酶(AMPK)激活剂和KATP通道打开剂均可引起常压条件下的心动过缓;然而,这些系统的假定拮抗剂未能预防或改善缺氧诱导的心动过缓。这表明一个或多个这些系统的激活并不是观察到的缺氧诱导的心动过缓的主要原因。在常氧条件下,氧化磷酸化的抑制也会降低HR,这突出了ATP水平的重要性。β受体阻滞剂美托洛尔引起HR浓度依赖性降低,支持β1-肾上腺素能受体存在于早期大鼠胚胎心脏的报道。cAMP诱导剂色forsin在常氧和缺氧条件下均诱导正向变时效应。总的来说,这个发育阶段的胚胎HR对氧合水平有反应,这可能是其对ATP产生影响的结果。
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