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A Journal on Surgery
Indexed/Abstracted in: EMBASE, Scopus, Emerging Sources Citation Index
Chirurgia 2012 February;25(1):11-9
Delayed myocardial protection by non-invasive limb ischemic preconditioning inhibits cardiomyocyte apoptosis and the fibrolysis system
Li S.-J. 1, 2, Wu Y.-N. 1, Kang Y. 1, Yin Y.-Q. 1, Gao W.-Z. 1, Liu Y.-X. 1, Lou J.-S. 1
1 Department of Pharmacology, Tianjin Medical University, Tianjin, China;
2 Pharmaceutical Preparation Section, Tianjin First Center Hospital, Tianjin, China
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.