Mechanism of Cardioprotective Effect of Remote Aortic Preconditioning

Summary

The present study is designed to investigate the mechanism of cardioprotective effect of remote aortic preconditioning. Four episodes, each episode comprising of 5min aortic occlusion followed by reperfusion for 5min were employed to produce remote preconditioning. Heart was isolated, perfused on Langendorff’s apparatus and subjected to 30 min of sustained global ischaemia followed by reperfusion for 120min. Coronary effluent was analysed for LDH and CK release to assess the degree of cardiac injury. Myocardial infarct size was estimated macroscopically using TTC staining. Remote aortic preconditioning reduced release of LDH and CK in coronary effluent and decreased myocardial infarct size. Reserpine, a biogenic amine depletor, ruthenium red, a sarcoplasmic reticulum Ca²⁺ channel blocker, ethylisopropylamiloride, (EIPA) a Na⁺/H⁺ exchange inhibitor and gadolinium, a mechanosensitive channel blocker, did not modulate the cardioprotective effect of remote aortic preconditioning. On the other hand, verapamil, a L type Ca²⁺ channel blocker, and 2′,4′-dichlorobenzamil, a Na⁺/Ca²⁺ exchange inhibitor, attenuated the cardioprotective effect of remote aortic preconditioning. On the basis of these results, it may be suggested that the cardioprotective effect of remote aortic preconditioning may be mediated through opening of L-type Ca²⁺ channels or activation of Na⁺/ Ca²⁺ exchange.