Transient depression of responses to sympathetic nerve stimulation overlying a subendocardial infarct

Abstract

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)