Role of mitochondrial permeability transition pore in cardioprotection by remote preconditioning.
- Author:
Yang CAO
1
;
Shi-Zhong ZHANG
;
Qiang XIA
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Extremities; blood supply; Ischemic Preconditioning; methods; Male; Mitochondrial Membrane Transport Proteins; physiology; Myocardial Reperfusion Injury; physiopathology; prevention & control; Rats; Rats, Sprague-Dawley
- From: Chinese Journal of Applied Physiology 2009;25(4):516-520
- CountryChina
- Language:Chinese
-
Abstract:
AIMTo investigate the role of mitochondrial permeability transition pore (MPTP) in the cardioprotection by remote preconditioning (RPC).
METHODSRemote 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.
RESULTSRPC 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).
CONCLUSIONInhibition of MPTP opening is involved in the cardioprotection by RPC.
