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首页> 外文期刊>Acta physiologica >Modulation of rabbit sinoatrial node activation sequence by acetylcholine and isoproterenol investigated with optical mapping technique.
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Modulation of rabbit sinoatrial node activation sequence by acetylcholine and isoproterenol investigated with optical mapping technique.

机译:光学映射技术研究了乙酰胆碱和异丙肾上腺素对兔窦房结激活序列的调控。

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AIMS: Changes in the rabbit sinoatrial node (SAN) activation sequence with the cholinergic and adrenergic factors were studied. The correlation between the sinus rhythm rate and the leading pacemaker site shift was determined. The hypothesis concerning the cholinergic suppression of nodal cell excitability as one of the mechanisms associated with pacemaker shift was tested. METHODS: A high-resolution optical mapping technique was used to register beat-to-beat changes in the SAN activation pattern under the influence of the cholinergic and adrenergic factors. RESULTS: Acetylcholine (10 microm) and strong intramural parasympathetic nerve stimulation caused a pacemaker shift as well as rhythmic slowing and the formation of an inexcitable region in the central part of SAN. In this region the generation of action potentials was suppressed. The slowing of the sinus rhythm (which exceeded 12.8 +/- 3.1% of the rhythm control rate) always accompanied the pacemaker shift. Isoproterenol (10, 100 nm, 1 microm) and sympathetic postganglionic nerve stimulation also evoked a pacemaker shift but without formation of an inexcitable zone. The acceleration of the sinus rhythm, which exceeded 10.5 +/- 1.3% of the control rate of the rhythm, always accompanied the shift. CONCLUSIONS: Both cholinergic and adrenergic factors cause pacemaker shifts in the rabbit SAN. While modest changes in the sinus rhythm do not coincide with the pacemaker shift, greater changes always accompany the shift and may be caused by it, according to one hypothesis. The formation of an inexcitable zone at the place where the leading pacemaker is situated is one of the mechanisms associated with pacemaker shift.
机译:目的:研究家兔窦房结(SAN)激活序列随胆碱能和肾上腺素能因子的变化。确定了窦性心律率与起搏器前移位置之间的相关性。测试了关于节细胞兴奋性胆碱能抑制作为与起搏器移位相关的机制之一的假说。方法:采用高分辨率光学映射技术记录胆碱能和肾上腺素能因子影响下SAN激活模式的逐搏变化。结果:乙酰胆碱(10微米)和强烈的壁内副交感神经刺激引起起搏器移位以及节律性减慢,并在SAN的中部形成了一个不可兴奋的区域。在该区域中,动作电位的产生被抑制。窦性心律减慢(超过心律控制率的12.8 +/- 3.1%)始终伴随着起搏器移位。异丙肾上腺素(10、100 nm,1微米)和交感神经节后神经刺激也引起起搏器移位,但没有形成无法激发的区域。窦性心律的加速总是伴随着移位,超过了心律控制率的10.5 +/- 1.3%。结论:胆碱能和肾上腺素能因素均会引起兔SAN起搏器移位。根据一种假设,虽然窦性心律的适度变化与起搏器移位并不吻合,但较大的变化总是伴随着移位,并且可能是由移位引起的。心脏起搏器所在的地方形成一个不可激励的区域,这是与心脏起搏器移位相关的机制之一。

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