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Updated: Jun 6, 2026

A Murine Closed-chest Model of Myocardial Ischemia and Reperfusion
Published on: July 17, 2012
[Role of mitochondrial permeability transition pore in cardioprotection by remote preconditioning]
Yang Cao1, Shi-Zhong Zhang, Qiang Xia
1Medical Science College of China Three Gorges University, Yichang 443002, China.
Aim:
To investigate the role of mitochondrial permeability transition pore (MPTP) in the cardioprotection by remote preconditioning (RPC).
Methods:
Remote Precondition (RPC) was induced in anesthetized male Sprague-Dawley rats by three cycles of 5 min of right femoral artery occlusion followed by 5 min of reperfusion. Myocardial ischemia/reperfusion (I/R) injury was achieved by ligation of the left anterior descending coronary artery for 30 min and then reperfusion for 120 min. Infarct size was determined by 2,3,5-triphenyltetrazolium chloride (TTC) staining method. The level of lactate dehydragenase (LDH) in plasma and the opening of the mitochondrial permeability transition pore (MPTP) were measured.
Results:
RPC significantly decreased the infarct size and plasma lactate dehydrogenase level induced by I/R, and these effects were attenuated by atractyloside (Atr, 5 mg/kg), a MPTP activator. However, administration of cyclosporin A (CsA, 10 mg/kg), an inhibitor of MPTP, decreased the effect of I/R. In isolated ventricular myocytes loaded with calcein, RPC decreased the MPTP opening, and this effect was attenuated by Atr (20 micromol/L).
Conclusion:
Inhibition of MPTP opening is involved in the cardioprotection by RPC.
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