Effects of pinacidil on electrophysiological properties of epicardial border zone of healing canine infarcts possible effects of KATP channel activation

James Coromilas, Constantinos Costeas, Bernard Deruyter, Stephen M. Dillon, Nicholas S. Peters, Andrew L. Wit

Research output: Contribution to journalArticlepeer-review

17 Scopus citations

Abstract

Background - KATP channels, activated by ischemia, participate in the arrhythmogenic response to acute coronary occlusion. The function of these channels in border zones of healing infarcts, where arrhythmias also arise, has not been investigated. Do these channels remain maximally activated during infarct healing, or do they downregulate after a period of time? Both might preclude further activation. Methods and Results - Myocardial infarction was produced in dogs by ligation of the left anterior descending coronary artery. Impulse propagation in the epicardial border zone (EBZ) of 4-day-old healing infarcts was mapped during administration of pinacidil, a KATP channel activator, directly into the EBZ coronary blood supply. Pinacidil restored conduction and excitability when the EBZ was initially inexcitable and had large regions of block (6 of 8 experiments). This allowed reentrant circuits to form in the EBZ, causing tachycardia (4 of 8 experiments). In hearts with an initially excitable EBZ, pinacidil shortened the effective refractory period and abolished conduction block at short cycle lengths (7 experiments). This effect prevented initiation of reentry (1 of 2 experiments). Conclusions - The response to pinacidil indicates that KATP channels in the EBZ remain functional and can be activated to influence electrophysiological properties and arrhythmogenesis.

Original languageEnglish (US)
Pages (from-to)2309-2317
Number of pages9
JournalCirculation
Volume105
Issue number19
DOIs
StatePublished - May 14 2002
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Keywords

  • Arrhythmia
  • Infarction
  • Ischemia

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