Delayed myocardial protection by non-invasive limb ischemic preconditioning inhibits cardiomyocyte apoptosis and the fibrolysis system

Aim. Our past research has shown that transient limb ischemia can induce remote late preconditioning that protects the myocardium from ischemia/reperfusion (I/R). In this study, we further tested if late preconditioning by non-invasive limb ischemia (NLIP) could offer cardioprotective effects against myocardium I/R injury. Methods. Sixty male Wistar rats weighing 240-260 g were randomly divided into the three following groups: I/R, cardiac ischemic preconditioning (CIP), and NLIP. Myocardial infarct size, myocardial apoptosis after prolonged I/R, and the levels of the controlling genes Bcl-2 and Bax were determined at the end of the experiment. The activity of fibrolysis factors, cardiac troponin I (cTnI) and superoxide dismutase (SOD) were measured before ischemia, after ischemia, and after reperfusion. Results. Myocardial infarct size was significantly reduced in the CIP and NLIP groups as compared with the I/R group (P<0.01). Pretreatment with CIP and NLIP significantly decreased the number of apoptotic cells (P<0.05), and the ratio of Bcl-2/Bax was increased (P<0.05). Compared with the I/R group, CIP and NLIP antagonized the decrease in t-PA activity (P<0.05) and the increase in PAI-1 activity (P<0.05), as well as the decrease in cTnI activity (P<0.01) and increase in SOD activity (P<0.05) after reperfusion. Conclusion. Remote preconditioning induced by NLIP provides late cardioprotection against myocardium I/R injury.