Objective To investigate the effect of peroxisome proliferatoractivated receptor-γ coactivator-1α(PGC-1α) on early ischemic preconditioning (IPC) which may act as an important role in early IPC. Methods Building isolated working rat heart Langendorff model, thirty Wistar rats were divided randomly into three groups. Control group(CON group,n=10): a 120-min perfusion was performed without any intervension; ischemia and reperfusion group(I/R group,n=10): a 30-min equilibration period perfusion, a 30-min ischemia and a 60-min reperfusion were performed.; IPC group (n=10): a 10-min equilibration period perfusion was performed, then was elicited by two cycles of 5-min of ischemia interspersed with 5-min reperfusion prior to 30-min ischemia and a 60-min reperfusion. Frozen sections of myocardium at cardiac apex were made and immunohistochemical staining was used to detect expression and the intergrated optical density average (IODA) of PGC-1α. Ultrathin sections were made and the mitochondria under each specimen was evaluated according to Flameng score. Results PGC-1α expression in IPC group (IODA 10.94±5.23) was significantly higher than that in I/R group (IODA 3.88±1.72) and that in CON group (IODA 3.39±2.46; P=0.009, 0.007). The mitochondria changes in I/R group were significant edema and severe damage; but there were not so severe in CON group and IPC group.Flameng score of IPC group (0.44±0.13) and CON group (0.88±0.22) were lower than that in I/R group(1.78±0.14;P=0.003, 0.014) respectively. Conclusion IPC can protect myocytes mitochondria from ischemia and reperfusion.The cardioprotection may be related with the activation and the high expression of PGC-1α, which may act as one of the most important endogenous defence factors of the heart.
ObjectiveTo investigate whether emulsified isoflurane applied after an ischemic episode induces postconditioning in an ischemia model of myocardial injury and its underlying mechanism. MethodsBetween March and October 2012, using a model of in situ myocardial ischemia and reperfusion injury in rats, cardioprotective effects of emulsified isoflurane were examined by determining infarct size, myocardial damage markers and the concentration of tumor necrosis factor (TNF)-α. ResultsEmulsified isoflurane postconditioning limited infarct size compared with control groups. It increased serum concentrations of superoxide dismutase while decreased malonaldehyde. TNF-α positive cells were also significantly reduced in emulsified isoflurane group compared with control group. Infusion of intralipid had no effect on infarct size or other variables. ConclusionIntravenous administration of emulsified isoflurane after reperfusion protects hearts against reperfusion injury, which may be mediated by the inhibition of cardiac damage markers and the concentration of TNF-α.