AJP - Heart and Circulatory Physiology, Vol 264, Issue 6 1969-H1976, Copyright © 1993 by American Physiological Society
Transient depression of responses to sympathetic nerve stimulation overlying a subendocardial infarct
J. B. Martins, D. G. Cable, T. E. Rath, L. Hingtgen, M. Horn and D. D. Lund
Department of Internal Medicine, University of Iowa, College of Medicine, Iowa City 52242.
In previous work, the normal epicardial rim overlying a subendocardial
infarct was demonstrated to be parasympathetically denervated. In the
present study, we determined responses of effective refractory period (ERP)
in this rim during sympathetic nerve stimulation (SNS). Eighteen dogs were
studied 1-3 days after a 1-h or permanent coronary artery occlusion (group
I). SNS shortened ERP in sites basal, septal, and lateral in the rim by 8
+/- 2, 7 +/- 2, and 7 +/- 2% (SE), respectively, which were similar to
sites remote from the infarct (10 +/- 1%). These results were not altered
by site of infarction or by atropine administration. To eliminate
dissection of the coronary vessel and spontaneous ventricular tachycardia,
19 dogs were studied 6 h after a permanent bead embolization of a coronary
artery (group II). In contrast to group I, ERP shortening in the rim sites
of group II was depressed (3 +/- 3, 0 +/- 2, and 1 +/- 2%, respectively)
compared with remote sites (10 +/- 1%, P < 0.05). In this group,
collateral blood flow in the rim was no different than remote epicardium
before and during SNS, and norepinephrine shortened ERP in the rim
equivalent to remote sites. In an additional 31 animals (group III), the
alteration in ATP-dependent K+ channel function was evaluated. Pretreatment
with glyburide (an ATP-dependent K+ channel blocker) preserved ERP response
to SNS (9 +/- 1% shortening of ERP vs. 12 +/- 2% at baseline) compared with
only 3 +/- 0% shortening of ERP with vehicle (P < 0.05).(ABSTRACT
TRUNCATED AT 250 WORDS)
