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1 Department of Cardiology, Hospital General Vall d'Hebron, Barcelona 08035, Spain; and 2 Department of Pharmacology, University College of Cork, Ireland
During myocardial ischemia, severe ATP
depletion induces rigor contracture followed by intracellular
Ca2+ concentration ([Ca2+]i) rise
and progressive impairment of gap junction (GJ)-mediated electrical
coupling. Our objective was to investigate whether chemical coupling
through GJ allows propagation of rigor in cardiomyocytes and
whether it persists after rigor development. In end-to-end connected
adult rat cardiomyocytes submitted to simulated ischemia the
interval between rigor onset was 3.7 ± 0.7 s, and subsequent [Ca2+]i rise was virtually identical in both
cells, whereas in nonconnected cell pairs the interval was 71 ± 12 s and the rate of [Ca2+]i rise was
highly variable. The GJ blocker 18
-glycyrrhetinic acid increased the
interval between rigor onset and the differences in
[Ca2+]i between connected cells. Transfer of
Lucifer yellow demonstrated GJ permeability 10 min after rigor onset in
connected cell pairs, and 30 min after rigor onset in isolated rat
hearts submitted to nonflow ischemia but was abolished after
2 h of ischemia. GJ-mediated communication allows
propagation of rigor in ischemic myocytes and persists after
rigor development despite acidosis and increased [Ca2+]i.
propagation; rigor contracture; calcium
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