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Basic science: Cardiovascular disease basic research
e0042 The effect of ischaemic postconditioning on the structure, function and Cx43 of mitochondria in rabbit myocardial isehemia/reperfusion injury
  1. Yan He,
  2. Zhi-Yu Zeng,
  3. Guo-Qiang Zhong,
  4. Wei Li,
  5. Wei-Ke Li
  1. Department of Cardiology, The First Affiliated Hospital of Guangxi Medical University

Abstract

Objective To investigate the effects of ischaemic postconditioning on structural and functional and connexin 43(Cx43) changes of mitochondria induced by myocardial ischaemia reperfusion (IR) injury of rabbits in vivo and potential mechanism.

Methods In anaesthetised open-chest rabbits, the left anterior descending artery (LAD) was occluded for 30 min and reperfused for 4 h. Sixty-four rabbits were randomly divided into four groups (n=16 in each group): Sham operation group (Group Sham), ischaemic reperfusion group (Group IR), ischaemic preconditioning group (Group IP) and ischaemic postconditioning group (Group PC) with sixteen rabbits in each. All rabbits in the four groups were killed 4 h after reperfusion. Myocardial infarct size were determined at the end of the experiment. Mitochondria were isolated with different centrifugations. Ultrastructural changes of mitochondria were observed under electronmicroscope and mitochondrial membrane potential, Ca2+ concentration, MDA content and SOD activity of myocardial mitochondria were examined. The content of the mitochondria Cx43 were detected with Western Blot.

Results Myocardial infarct size was significantly reduced in IP (18.9±2.8)%)and PC (19.1±3.9)%)groups as compared to IR groups (35.7±5.8)%, p<0.01). Compared with group IR, the damage of mitoehondrial ultrastrueture were milder and Ca2+ concentration and MDA content were much lower in group IP and group PC (p<0.05). Mitochondrial membrane potential (p<0.01) and SOD activity of myocardial mitochondria in group IP and group PC was significantly higher than that in group IR (p<0.05). Compared with sham group, the mitochondria Cx43 expression is distinctly decreased compared group IR (p<0.05) and no significant difference was found between Group IP and Group PC.

Conclusion PC can protect mitochondrial ultrastructure by increaseing mitochondrial membrane potential and SOD activity, and by alleviating Ca2+ overload, and by decreasing MDA content in myocardial mitochondria. The mechanism of PC protection to mitochondria may be concerned with PC attenuating the decrease the mitochondria Cx43 expression induced by ischaemia/reperfusion injury.

  • Ischaemia reperfusion
  • postconditioning
  • mitochondria
  • myocardial
  • connexin 43

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