Pretreatment with the gap junction uncoupler heptanol does not limit infarct size in rabbit heart

Anne Gysembergh, Robert A. Kloner, Karin Przyklenk

Research output: Contribution to journalArticlepeer-review

21 Scopus citations


Previous findings indicate that heptanol, an agent well-recognized to disrupt chemical signaling between myocytes by uncoupling of gap junctions, significantly limited infarct size when administered at the time of reperfusion. Our aim was to assess on the potential role of cell-cell communication via gap junctions during ischemia by investigating whether 'loading' the soon-to-be ischemic territory with heptanol would limit myocardial necrosis. Five isolated buffer-perfused rabbit hearts were pretreated with heptanol (0.5 mM) for 10 min, while 12 served as controls. In the final 30 s of treatment, a large marginal branch of the left circumflex coronary artery was occluded for 30 min followed by 2 h of reperfusion, and infarct size was delineated by tetrazolium staining. Heptanol had no significant effect on the extent of infarct: area of necrosis (AN, expressed as a percentage of the myocardium at risk) was 75±3% and 72±8% in vehicle- and heptanol-treated groups (P=.76). Thus, our results suggest that cell-to-cell communication via gap junctions during coronary artery occlusion does not contribute importantly to the development of necrosis in rabbit heart.

Original languageEnglish
Pages (from-to)13-17
Number of pages5
JournalCardiovascular Pathology
Issue number1
StatePublished - Jan 2 2001


  • Calcium
  • Gap junctions
  • Myocardial ischemia
  • Myocordial infarction


Dive into the research topics of 'Pretreatment with the gap junction uncoupler heptanol does not limit infarct size in rabbit heart'. Together they form a unique fingerprint.

Cite this