AJP - Heart and Circulatory Physiology, Vol 253, Issue 2 333-H340, Copyright © 1987 by American Physiological Society
Postpacing tachycardia: autonomic involvement
J. M. Loeb, J. M. deTarnowsky, M. R. Warner and C. C. Whitson
The cessation of pacing from the sinus node region is followed by a
transient sinus tachycardia or postpacing tachycardia (PPT). We sought to
characterize autonomic involvement in PPT. We used
alpha-chloralose-anesthetized dogs and recorded electrocardiograms, blood
pressure, and electrograms from the sinus node, right atrium, right
ventricle, and His bundle. Both vagi and both stellate ganglia were
transected. PPT developed immediately after either linear or stepped heart
rate changes. PPT followed pacing from the rostral but not the caudal
region of the sulcus terminalis. Independent manipulation of absolute level
of heart rate (+33, +66, and +100 beats/min above control) and duration of
atrial pacing (10, 20, and 30 s) revealed that PPT is dependent
predominantly on the duration of pacing and less on level of heart rate.
During pacing in the control state, a 1:1 atrial capture was maintained.
After atropine administration (0.2 mg/kg iv), PPT increased significantly
in magnitude, time to peak PPT was shortened significantly, and loss of 1:1
atrial capture during pacing was evident at pacing rates of from 10 to 60
beats above control. In contrast, propranolol significantly attenuated PPT.
We conclude that acetylcholine, released during pacing from the sinus node
region, suppresses inherent sinus node acceleration induced by the
concurrent release of intramural catecholamines. During pacing,
acetylcholine release is essential for the maintenance of 1:1 atrial
capture and significantly modulates both the latency and magnitude of PPT.
