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 disru pt chemical signaling between myocytes by uncoupling of gap junctions, sign ificantly limited infarct size when administered at the time of reperfusion . Our aim was to assess on the potential role of cell-cell communication vi a gap junctions during ischemia by investigating whether "loading" the soon -to-be ischemic territory with heptanol would limit myocardial necrosis. Fi ve 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 treatme nt, a large marginal branch of the left circumflex coronary artery was occl uded for 30 min followed by 2 h of reperfusion, and infarct size was deline ated by tetrazolium staining. Heptanol had no significant effect on the ext ent of infarct: area of necrosis (AN, expressed as a percentage of the myoc ardium at risk) was 75 +/- 3% and 72 +/- 8% in vehicle- and heptanol-treate d groups (P=.76). Thus, our results suggest that cell-to-cell communication via gap junctions during coronary artery occlusion does not contribute imp ortantly to the development of necrosis in rabbit heart. (C) 2001 Elsevier Science Inc. All rights reserved.