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1 Servicio de Cardiologia. Laboratorio de Cardiologia Experimental, Hospital Vall d'Hebron, Barcelona, Barcelona, Spain
* To whom correspondence should be addressed. E-mail: dgdorado{at}vhebron.net.
The end-effectors of ischemic preconditioning (IPC) are not well known. It has been recently shown that transgenic mice underexpressing the gap junction (GJ) protein Cx43 cannot be preconditioned. Since GJs allow spreading of cell death during ischemia-reperfusion in different tissues, including myocardium, we hypothesized that the protection afforded by IPC is mediated by effects on GJ-mediated intercellular communication. To test this hypothesis, we analyzed the effect of IPC (5 min ischemia-5min reperfusion x2) on the changes in electrical impedance (four electrode probe) and impulse propagation velocity (transmembrane action potential) induced by ischemia (60 min) and reperfusion (60 min) in isolated rat hearts. IPC (n=8) reduced reperfusion-induced LDH release by 65.8% respect to control hearts (n=9) (p=0.04), but had no effect on the time of onset of rigor contracture (increase in diastolic tension), electrical uncoupling (sharp changes in tissue resistivity and phase angle in impedance recordings) or block of impulse propagation during ischemia. Normalization of electrical impedance during reperfusion was also unaffected by IPC. The lack of effect of IPC on ischemic rigor contracture and on changes in tissue impedance during ischemia-reperfusion were validated under in vivo conditions in pigs submitted to 48min of coronary occlusion and 120min of reperfusion. IPC (n=12) reduced infarct size (triphenyltetrazolium) by 64.9% (p=0.01) respect controls (n=17). We conclude that the protection afforded by IPC is not mediated by effects on electrical coupling. This result is consistent with recent findings suggesting that Cx43 could have effects on cell survival independent of changes in cell-to-cell communication.
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