Key result
Surgical ablation of the posterior atrial ganglionated plexus in dogs significantly increased peak tachycardia to a stressful stimulus from +53 to +77 beats/min (P<0.05).
Why the study?
Does ablation of the posterior atrial ganglionated plexus increase sympathetic tachycardia to behavioral stress in unanesthetized dogs?
Does ablation of the posterior atrial ganglionated plexus increase sympathetic tachycardia to behavioral stress in unanesthetized dogs?
Absolute Event Rate: 77% vs 53%
p-value: p=< 0.05
Ablation of the posterior atrial ganglionated plexus augments sympathetic tachycardia during behavioral stress, indicating that its parasympathetic neurons normally inhibit sympathoexcitatory effects on the sinoatrial node.
PAGP ablation augments stress tachycardia in dogs without altering resting HR; leaves open its role in human autonomic regulation.
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 beta-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.
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Randall et al. (1998) studied this question. Surgical ablation of posterior atrial ganglionated plexus (PAGPX) vs. Before ablation (baseline) was evaluated on Peak tachycardia to a 30-s stressful stimulus (p=< 0.05). Surgical ablation of the posterior atrial ganglionated plexus in dogs significantly increased peak tachycardia to a stressful stimulus from +53 to +77 beats/min (P<0.05).
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