Reflex vagal control of atrial repolarization.
Euler, David E., Brian Olshansky, and Shin Y. Kim.
Section of Cardiology, Department of Medicine, Loyola University
Medical Center, 2160 South First Avenue, Maywood, IL 60153
APStracts 3:0051H, 1996.
The reflex vagal control of atrial repolarization was investigated in
eight open-chest anesthetized dogs. A monophasic action potential was
recorded from the right atrium and the time to 90% repolarization
(APD90) was determined every cardiac cycle. Beta-adrenergic receptors
were blocked with timolol (0.1 mg/kg). Under baseline conditions,
sinus slowing during sinus arrhythmia was accompanied by a
significant shortening of APD90 (24 +/- 4.0 msec). Transient
occlusion (30 seconds) of the descending thoracic aorta increased
systolic arterial pressure from 138 +/- 2.8 to 181 +/- 3.3 mmHg
(P<0.01). Heart rate decreased from 99 +/- 3.6 to 42.5 +/- 3.4
beats/min (P<0.01) and APD90 shortened from 168 +/- 5.1 to 94
+/- 3.3 msec (P<0.01). Release of the occlusion caused arterial
hypotension (95 +/- 2.8 mmHg) and an overshoot in both rate (126 +/-
5.2 beats/min) and APD90 (189 +/- 2.3 msec). Aortic occlusion during
atrial pacing (130-160 beats/min) decreased APD90 from 147 +/- 7.0 to
78 +/- 3.4 msec (P<0.01) . Cervical vagotomy or atropine
eliminated changes in rate and APD90 evoked by aortic occlusion. The
results indicate that there is parallel central vagal control of both
sinus rate and atrial repolarization. Sinus bradycardia during reflex
vagal activation does not prevent the acceleration of atrial
repolarization.
Received 4 October 1995; accepted in final form 18 January 1996.
APS Manuscript Number H934-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 8 February 96