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Effect of verapamil on conduction delay produced by myocardial ischemia and reperfusion.

Abstract：

:Changes in conduction times induced by ischemia (delta CT) have been shown to be quantitatively related to genesis of spontaneous ischemic ventricular fibrillation (VF). We studied conduction delay encountered by premature impulses in epicardium and endocardium in both anterograde and retrograde directions during ischemia and reperfusion in eight control and in eight verapamil treated dogs. Acute myocardial ischemia was produced by single-stage ligation of left anterior descending artery below second diagonal initially, and 30 minutes later below first diagonal branch. In treated dogs, verapamil was given, 0.15 mg/kg intravenous bolus, immediately after first ligation and was followed by an infusion of 7.5 micrograms/kg/min. Thus post-treated segment and pretreated segment were obtained in the same animal. delta CT was compared between control and treated dogs in four myocardial zones: (1) normal, (2) ischemic including pre- and post-treated segments, (3) reperfused, and (4) border of reperfusion or ischemia. Results showed that ischemia-induced conduction delay was significantly less in verapamil treated dogs throughout period of ischemia and reperfusion, both in epicardium and endocardium. In addition, in the border of ischemia retrograded conduction showed significantly less depression during ischemia and reperfusion. The protective effect of verapamil was impressive both in pretreated and post-treated segments of ischemic myocardium. We conclude that verapamil offers significant protective action with regard to ischemia-induced conduction delay. Since delta CT is quantitatively related to ischemic VF, verapamil can be antiventricular fibrillatory in myocardial ischemia.

journal_name

Am Heart J

journal_title

American heart journal

authors

Hamamoto H,Peter T,Fujimoto T,Mandel WJ

doi

10.1016/0002-8703(81)90308-2

subject

Has Abstract

pub_date

1981-09-01 00:00:00

pages

350-8

issue

3 Pt 1

eissn

0002-8703

issn

1097-6744

pii

0002-8703(81)90308-2

journal_volume

102

pub_type

杂志文章

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