OBJECTIVE: To investigate the roles of mitochondrial connexin43 (Cx43) and mitochondrial ATP sensitive potassium channe1 (mitoK(ATP)+) in the postconditioning protection for rabbits underwent myocardial ischemia/reperfusion injury. METHODS: In anesthetized open-chest rabbits, the left anterior descending artery (LAD) was occluded for 30 min and reperfused for 4 h and randomly divided into four groups (n = 16 each): sham operation group (Sham), ischemic reperfusion group (IR), ischemic postconditioning group (PC) and PC plus 5-HD, a specific mitoK(ATP)+ inhibitor (PC + 5-HD). Rabbits were sacrificed post 4 h reperfusion. Heart rate and the mean arterial pressure were recorded and plasma CK-MB and cTnI activity were measured at baseline, at the end of ischemia, and after 2 h and 4 h of reperfusion, respectively. Myocardial infarct size was determined and mitochondria structure was observed under electron microscope at the end of the experiment. Mitochondria were isolated and the protein content of the mitochondrial Cx43 was determined by Western blot. RESULTS: Plasma CK-MB, cTnI activity and myocardial infarct size were significantly reduced in PC [(19.1 +/- 3.9)%] group compared to IR [(35.7 +/- 5.8)%] and PC + 5HD [(34.2 +/- 3.9)%] groups (all P < 0.01). Degree of mitochondria damage was significantly reduced in PC group compared to IR and PC + 5HD groups (all P < 0.01). The mitochondria Cx43 content was significantly decreased in IR group and PC + 5-HD group compared to sham group (all P < 0.05) and restored in PC group. CONCLUSION: Ischemic postconditioning protected the heart from I/R injury by improving mitochondrial ultrastructure and by attenuating I/R induced decrease of mitochondria Cx43 expression. The protective effects of postconditioning was partly mediated by activating mitoK(ATP)+ pathway.
OBJECTIVE: To investigate the roles of mitochondrial connexin43 (Cx43) and mitochondrial ATP sensitive potassium channe1 (mitoK(ATP)+) in the postconditioning protection for rabbits underwent myocardial ischemia/reperfusion injury. METHODS: In anesthetized open-chest rabbits, the left anterior descending artery (LAD) was occluded for 30 min and reperfused for 4 h and randomly divided into four groups (n = 16 each): sham operation group (Sham), ischemic reperfusion group (IR), ischemic postconditioning group (PC) and PC plus 5-HD, a specific mitoK(ATP)+ inhibitor (PC + 5-HD). Rabbits were sacrificed post 4 h reperfusion. Heart rate and the mean arterial pressure were recorded and plasma CK-MB and cTnI activity were measured at baseline, at the end of ischemia, and after 2 h and 4 h of reperfusion, respectively. Myocardial infarct size was determined and mitochondria structure was observed under electron microscope at the end of the experiment. Mitochondria were isolated and the protein content of the mitochondrial Cx43 was determined by Western blot. RESULTS: Plasma CK-MB, cTnI activity and myocardial infarct size were significantly reduced in PC [(19.1 +/- 3.9)%] group compared to IR [(35.7 +/- 5.8)%] and PC + 5HD [(34.2 +/- 3.9)%] groups (all P < 0.01). Degree of mitochondria damage was significantly reduced in PC group compared to IR and PC + 5HD groups (all P < 0.01). The mitochondria Cx43 content was significantly decreased in IR group and PC + 5-HD group compared to sham group (all P < 0.05) and restored in PC group. CONCLUSION:Ischemic postconditioning protected the heart from I/R injury by improving mitochondrial ultrastructure and by attenuating I/R induced decrease of mitochondria Cx43 expression. The protective effects of postconditioning was partly mediated by activating mitoK(ATP)+ pathway.