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

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 vi...

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Bibliographic Details
Published in:Cardiovascular pathology 2001-01, Vol.10 (1), p.13-17
Main Authors: Gysembergh, Anne, Kloner, Robert A, Przyklenk, Karin
Format: Article
Language:English
Subjects:
Animals
Calcium
Coronary Circulation - drug effects
Gap junctions
Gap Junctions - drug effects
Heart - drug effects
Heart - physiopathology
Hemodynamics - drug effects
Heptanol - pharmacology
In Vitro Techniques
Male
Myocardial Infarction - pathology
Myocardial ischemia
Myocardial Reperfusion Injury - pathology
Myocardial Reperfusion Injury - physiopathology
Myocardial Reperfusion Injury - prevention & control
Myocordial infarction
Necrosis
Perfusion
Rabbits
Uncoupling Agents - pharmacology
Ventricular Dysfunction, Left - physiopathology
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Summary: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.
ISSN:1054-8807
1879-1336
DOI:10.1016/S1054-8807(00)00056-9