Author + information
- Received February 18, 1983
- Revision received August 9, 1983
- Accepted August 17, 1983
- Published online December 1, 1983.
- James B. Martins, MD*,
- Douglas P. Zipes, MD, FACC and
- Donald D. Lund, PhD
- ↵*Address for reprints: James B. Martins, MD, Cardiovascular Division, #318–3, Department of Medicine, University of Iowa Hospitals, Iowa City, Iowa 52242.
The purpose of this study was to compare the distribution of effects of right and left efferent vagal stimulation on ventricular recovery properties in the in situ heart. To measure these effects in many areas simultaneously, local repolarization changes (local QT intervals) were recorded with bipolar electrodes in nine ventricular sites from 38 anesthetized dogs. In initial experiments, this method was shown to correlate with effective refractory period changes measured in the same test site after QT recording; vagal nerve stimulation prolonged the local QT interval by 1 ms for each 0.82 ms prolongation in effective refractory period (r = 0.87).
Simultaneous local QT recordings during vagal nerve stimulation demonstrated uniform prolongation with two exceptions. First, left vagal efferent stimulation prolonged local QT interval in the posterior left ventricular base more than did right vagal stimulation (5.9 ± 1.0 mean ± standard error of the mean versus 3.7 ± 0.9%, p < 0.05). This probably resulted from an interaction with the left sympathetic nerves because left stellate gan-glionectomy or norepinephrine infusion eliminated differences between effects of right and left vagal stimulation. Second, it was also found that vagal stimulation from either side did not prolong local QT interval time in the anterior right ventricle despite attempts to augment vagal effects with bilateral vagal stimulation alone or during isoproterenol or physostigmine administration.
These regional differences in ventricular repolarization exhibited in response to efferent vagal nerve stimulation in the dog may provide a basis for understanding how autonomic influences could contribute to the genesis of ventricular arrhythmias.
This work was done during the tenure of a Clinician-Scientist Award from the American Heart Association, Inc., with funds contributed in part by the Iowa Heart Association, Des Moines, Iowa. In addition, support for this work also came from the National Institutes of Health (Grant HL 26567), Bethesda, Maryland and the Veterans Administration, Washington D.C.
- Received February 18, 1983.
- Revision received August 9, 1983.
- Accepted August 17, 1983.
- American College of Cardiology Foundation