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首页> 外文期刊>Journal of cardiovascular electrophysiology >Parasympathetic inhibition of sympathetic effects on pacemaker location and rate in hearts of anesthetized dogs.
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Parasympathetic inhibition of sympathetic effects on pacemaker location and rate in hearts of anesthetized dogs.

机译:副交感神经对麻醉狗心脏起搏器位置和速率的同情影响。

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INTRODUCTION: The site of impulse origin in the right atrium generally is considered to be a single static locus within the sinoatrial (SA) node. Previous investigators showed that the pacemaker site may shift due to changes in sympathetic or parasympathetic neural activity. We investigated the interactions between sympathetic and parasympathetic influences on the site of impulse initiation in the right atrium in anesthetized dogs. METHODS AND RESULTS: We determined the site of impulse initiation and the spread of excitation over the anterior and posterior regions of the right atrium by a matrix of 48 unipolar recording electrodes. We assessed the spread of excitation at 3-msec intervals by constructing isochronal activation sequence maps. Sympathetic stimulation increased the frequency of atrial excitation (i.e., the heart rate), but also shifted the earliest activation region (EAR) from a locus in the SA node to a locus in the superior vena cava (the superior pacemaker site). Vagus stimulation decreased the heart rate and shifted the EAR to a lower site in the SA node or a site in the inferior right atrium along the sulcus terminalis (the inferior pacemaker site). A short period of vagus stimulation during a more prolonged sympathetic stimulation elicited a larger decrease in rate than did vagus stimulation alone and shifted the EAR from the superior site to the SA node or to the inferior site. After atropine, combined stimulation shifted the EAR to the superior site, but propranolol did not change EAR location. CONCLUSION: Our results suggest that parasympathetic activity predominates over sympathetic activity not only on heart rate, but also on the location of the EAR in the anesthetized dog.
机译:简介:通常认为在右心房的冲动起源部位是窦房结(SA)内的单个静态位点。先前的研究人员表明,起搏器部位可能由于交感神经或副交感神经活动的变化而发生移位。我们调查了在麻醉犬的右心房冲动起始部位的交感和副交感影响之间的相互作用。方法和结果:我们通过48个单极记录电极的矩阵确定了右心房前部和后部区域的脉冲起始点和激发的分布。我们通过构建等时激活序列图来评估以3毫秒为间隔的激发传播。交感神经刺激增加了心房兴奋的频率(即心率),但也将最早的激活区域(EAR)从SA节点的部位转移到了上腔静脉(上起搏器部位)的部位。迷走神经刺激降低了心率,并使EAR移至SA结的较低部位或沿沟的右下心房部位(起搏器下方部位)。在更长时间的交感神经刺激中,短时间的迷走神经刺激比单独的迷走神经刺激引起更大的降低,并使EAR从上位转移到SA结或下位。阿托品后,联合刺激使EAR移至上位,但普萘洛尔并未改变EAR的位置。结论:我们的结果表明,副交感神经活动不仅在心率上而且在麻醉狗中EAR的位置上都优于交感神经活动。

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