Ablation of posterior atrial ganglionated plexus potentiates sympathetic tachycardia to behavioral stress.
Ablation of posterior atrial ganglionated plexus potentiates sympathetic tachycardia to behavioral stress.
复制标题
后心房神经节丛的消融会增强行为应激引起的交感性心动过速。
DOI：
10.1152/ajpregu.1998.275.3.r779
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发表时间：
1998
期刊：
影响因子：
--
通讯作者：
Ardell,JL
中科院分区：
文献类型：
--
作者：
Randall,DC;Brown,DR;Li,SG;Olmstead,ME;Kilgore,JM;Sprinkle,AG;Randall,WC;Ardell,JL
The role of the posterior atrial ganglionated plexus (PAGP) in heart rate (HR) control was tested in unanesthetized dogs (n= 8). Resting HR was unchanged before (85 ± 20 beats/min, mean ± SD) versus after (87 ± 18 beats/min) surgical ablation of these intrinsic cardiac ganglia (PAGPX). However, the peak tachycardia to a 30-s stressful stimulus was significantly increased (P< 0.05) from +53 ± 22 beats/min before the denervation to +77 ± 13 beats/min after PAGPX. Conversely, the peak HR increase during the stress after β-adrenergic blockade was the same before (36 ± 24 beats/min) versus after (38 ± 14 beats/min) PAGPX. Moreover, the HR response to a neutral behavioral stimulus, which is mediated primarily by withdrawal of parasympathetic inhibition of the sinoatrial (SA) node, was unaltered by PAGPX. Thus the augmented tachycardia subsequent to PAGPX was attributable primarily to increased sympathetic action at the SA node. These findings indicate that a major role of PAGP parasympathetic neurons is to inhibit sympathoexcitatory effects on HR, probably either via interactions between neurons comprising the intrinsic plexus(es) or perhaps via presynaptic inhibition of sympathetic neurotransmitter release. This organization would allow parasympathetic ganglia within the PAGP to selectively modify sympathetic input to the SA node independent of direct vagal inhibition of pacemaker activity.
