Persistence of gap junction communication during myocardial ischemia

During myocardial ischemia, severe ATP depletion induces rigor contracture followed by intracellular Ca2+ concentration ([Ca2+](i)) rise and progressi ve impairment of gap junction (GJ)-mediated electrical coupling. Our object ive was to investigate whether chemical coupling through GJ allows propagat ion of rigor in cardiomyocytes and whether it persists after rigor developm ent. In end-to-end connected adult rat cardiomyocytes submitted to simulate d ischemia the interval between rigor onset was 3.7 +/- 0.7 s, and subseque nt [Ca2+](i) rise was virtually identical in both cells, whereas in nonconn ected cell pairs the interval was 71 +/- 12 s and the rate of [Ca2+](i) ris e was highly variable. The GJ blocker 18 alpha -glycyrrhetinic acid increas ed the interval between rigor onset and the differences in [Ca2+](i) betwee n connected cells. Transfer of Lucifer yellow demonstrated GJ permeability 10 min after rigor onset in connected cell pairs, and 30 min after rigor on set in isolated rat hearts submitted to nonflow ischemia but was abolished after 2 h of ischemia. GJ-mediated communication allows propagation of rigo r in ischemic myocytes and persists after rigor development despite acidosi s and increased [Ca2+](i).