No loss of cardioprotection by postconditioning in connexin 43-deficient mice.
In situ hearts and isolated cardiomyocytes from heterozygous connexin 43-deficient (Cx43+/-) mice cannot be protected by ischemic preconditioning or diazoxide. We have now addressed the role of connexin 43 in ischemic postconditioning (PC). Wild type (WT) and Cx43+/- mice were subjected to 30 min coronary occlusion and 120 min reperfusion, with and without a PC protocol of three cycles of 10 s coronary occlusion/10 s reperfusion. Infarct size (TTC staining) was reduced by PC from 54+/-5 to 37+/-3% of area at risk in WT. Likewise, infarct size was reduced by PC from 53+/-4 to 34+/-3% of area at risk in Cx43+/-. We conclude that connexin 43 is no prerequisite for PC's protection. To this end, the signal transduction of ischemic preconditioning and postconditioning differs.
Heusch
Gerd
G
Institut für Pathophysiologie, Zentrum für Innere Medizin Universitätsklinikum Essen, Hufelandstr. 55, 45122, Essen, Germany. gerd.heusch@uni-essen.de
Büchert
Astrid
A
Feldhaus
Sandra
S
Schulz
Rainer
R
D000818:Animals; D018031:Connexin 43 / Q000502:physiology*; D006321:Heart / Q000502:physiology; D051379:Mice; D017202:Myocardial Ischemia / Q000473:pathology*; D015428:Myocardial Reperfusion Injury / Q000517:prevention & control*
D018031:Connexin 43