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.
Institut für Pathophysiologie, Zentrum für Innere Medizin Universitätsklinikum Essen, Hufelandstr. 55, 45122, Essen, Germany. gerd.heusch@uni-essen.de
Gerd
G
Heusch
Astrid
A
Büchert
Sandra
S
Feldhaus
Rainer
R
Schulz
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