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迷走神经刺激和硝普钠诱导绵羊胎儿低血压期间交感神经张力对心率的影响。

Influence of sympathetic tone on heart rate during vagal stimulation and nitroprusside induced hypotension in ovine fetus.

作者信息

Gaillot Théophile, Beuchée Alain, Jaillard Sophie, Storme Laurent, Nuyt Anne Monique, Carré François, Pladys Patrick

机构信息

Department of Pediatrics, CHU, Rennes, France.

出版信息

Auton Neurosci. 2005 Dec 30;123(1-2):19-25. doi: 10.1016/j.autneu.2005.08.001. Epub 2005 Oct 5.

Abstract

OBJECTIVE

To characterize effects of sympathetic tone on fetal heart rate (FHR) reflex responses and FHR variability in late gestation.

DESIGN/METHODS: Changes in FHR and autonomic tones were studied (i) after electrical vagal stimulation and (ii) during nitroprusside-induced hypotension, in seven late gestation ovine fetus in control condition (ctrl), after dobutamine (beta1-activation) and atenolol (beta1-blockade). Results are expressed as mean +/- SEM.

RESULTS

(i) Minimal FHR after vagal stimulation was not influenced by atenolol or dobutamine but dobutamine accelerated FHR normalization. (ii) During nitroprusside induced hypotension atenolol inhibited the initial increases in FHR and FHR variability (measured by SD and LFnu) but not the bradycardia occurring below a mean arterial pressure of 38 +/- 2 mmHg. Dobutamine did not abolish the depressor reflex. During hypotension the positive chronotropic effect of sympathetic tone increased from 15 +/- 2 to 42 +/- 7 bpm then decreased at a rate of -7.6 +/- 1.5 bpm mmHg(-1), vagal negative chronotropic influence steadily increased at a rate of 1.9 +/- 0.4 bpm mmHg(-1). Changes in FHR variability were not correlated with vagal or sympathetic chronotropic effects.

CONCLUSIONS

beta1-stimulation does not affect sinus-node response to vagal stimulation but improves the speed of FHR normalization. FHR response to hypotension depends on an initial increase in both sympathetic and parasympathetic chronotropic effects that is associated with a sympathetic dependent increase in FHR variability and is followed by a withdrawal of sympathetic tone.

摘要

目的

描述交感神经张力对妊娠晚期胎儿心率(FHR)反射反应及FHR变异性的影响。

设计/方法:在7只妊娠晚期绵羊胎儿处于对照状态(ctrl)时、给予多巴酚丁胺(β1激活)和阿替洛尔(β1阻断)后,研究了(i)电迷走神经刺激后及(ii)硝普钠诱导低血压期间FHR和自主神经张力的变化。结果以平均值±标准误表示。

结果

(i)迷走神经刺激后的最低FHR不受阿替洛尔或多巴酚丁胺影响,但多巴酚丁胺加速了FHR恢复正常。(ii)在硝普钠诱导的低血压期间,阿替洛尔抑制了FHR和FHR变异性(通过标准差和低频功率测量)的初始增加,但未抑制平均动脉压低于38±2 mmHg时出现的心动过缓。多巴酚丁胺未消除降压反射。在低血压期间,交感神经张力的正性变时作用从15±2次/分增加到42±7次/分,然后以-7.6±1.5次/分·mmHg-1的速率下降,迷走神经负性变时影响以1.9±0.4次/分·mmHg-1的速率稳步增加。FHR变异性的变化与迷走神经或交感神经变时作用无关。

结论

β1刺激不影响窦房结对迷走神经刺激的反应,但提高了FHR恢复正常的速度。FHR对低血压的反应取决于交感神经和副交感神经变时作用的初始增加,这与FHR变异性的交感神经依赖性增加相关,随后是交感神经张力的撤离。

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