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首页> 外文期刊>Journal of cardiovascular electrophysiology >Autonomic control of the location and rate of the cardiac pacemaker in the sinoatrial fat pad of parasympathetically denervated dog hearts.
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Autonomic control of the location and rate of the cardiac pacemaker in the sinoatrial fat pad of parasympathetically denervated dog hearts.

机译:副交感神经失调的狗心脏窦房脂肪垫中心脏起搏器位置和速率的自主控制。

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INTRODUCTION: Parasympathetic activity predominates over sympathetic activity not only with respect to heart rate but also with respect to the pacemaker location in the dog heart. After we removed the parasympathetic neural elements in the sinoatrial (SA) fat pad in the right atrium, we observed that cervical vagus stimulation did not decrease the atrial rate, but it did suppress the increase in rate evoked by sympathetic stimulation. We determined whether the pacemaker rate and location were affected by presynaptic or postsynaptic mechanisms. METHODS AND RESULTS: We determined the earliest activation site by means of isochronic activation mapping of the right atrium of open chest, anesthetized dog hearts. An electrode array, which consisted of 48 unipolar electrodes, was used to record atrial activation. This array covered the three main pacemaker regions, including the SA node region. After parasympathetic nerve fibers in the SA fat pad had been denervated, vagus stimulation at 10 and 30 Hz did not decrease the heart rate, but it attenuated the increase in heart rate evoked by sympathetic stimulation or isoproterenol. Vagus stimulation at 10 Hz during sympathetic stimulation did not shift the earliest activation site from the superior pacemaker region to the SA node region in 11 of 18 experiments. However, vagus stimulation at 10 Hz during isoproterenol infusion shifted the earliest activation site to the SA node region in 11 of 13 experiments. More intense vagus stimulation during combined sympathetic stimulation or isoproterenol infusion shifted the earliest activation site to the SA node or the inferior pacemaker region in 15 of 18 and in all experiments, respectively. CONCLUSION: The results suggest that activation of parasympathetic elements not located in the SA fat pad attenuates the increase in heart rate and the shift in pacemaker location evoked by sympathetic activation. The sympathetic and parasympathetic effects interact at presynaptic and postsynaptic sites in the dog heart.
机译:简介:交感神经活动不仅在心率方面而且在狗心脏中的起搏器位置方面都比交感神经活动重要。除去右心房窦房(SA)脂肪垫中的副交感神经元后,我们观察到宫颈迷走神经刺激并没有降低心房率,但确实抑制了交感刺激引起的心率增加。我们确定起搏器的速度和位置是否受到突触前或突触后机制的影响。方法和结果:我们通过等时激活图谱确定了麻醉后的开胸胸腔右心房的最早激活部位。电极阵列由48个单极电极组成,用于记录心房激活。该阵列覆盖了三个主要的起搏器区域,包括SA节点区域。去掉SA脂肪垫中的副交感神经纤维后,在10和30 Hz迷走神经刺激不会降低心率,但会减弱交感刺激或异丙肾上腺素引起的心率增加。在18个实验中的11个实验中,在交感刺激期间以10 Hz进行迷走神经刺激并未将最早的激活部位从上起搏器区域转移到SA结区域。然而,在13个实验中的11个实验中,在异丙肾上腺素输注过程中以10 Hz迷走神经刺激将最早的激活位点转移到了SA结区域。在联合交感刺激或异丙肾上腺素输注期间,更强烈的迷走神经刺激分别在18个实验中的15个和所有实验中将最早的激活位点转移到了SA结或起搏器下区域。结论:结果表明,未位于SA脂肪垫中的副交感神经元的激活减弱了心率的增加以及由交感神经激活引起的起搏器位置的改变。交感和副交感作用在犬心脏的突触前和突触后部位相互作用。

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