Aim This paper aims at investigating the effect of dofetilide on Na+/Ca 2+exchange in ventricular myocytes of adult guinea pigs. Methods Rapid enzymatic isolation procedure was performed to get single ventricular myocytes from adult guinea pigs. After the whole cell configuration was formed, a ramp voltage-clamp pulse depolarized from a holding potential of -40 mV to +60 mV, then hyperpolarized to -120 mV at a rate of 90 mV/s to record the Na+/Ca 2+ exchange current (I Na/Ca) and the influence of dofetilide from 0.03～1.0 ?mol?L -1. Result Dofetilide from 0.03～1.0 ?mol?L -1 concentration-dependently increased the I Na/Ca in both outward and inward mode. The EC 50 of dofetilide on I Na/Ca in outward and inward mode of NCE was 0.178 ?mol?L -1 (95% confidence interval was 0.040～0.787 ?mol?L -1) and 0.178 ?mol?L -1 (95% confidence interval was 0.038～0.842 ?mol?L -1), respectively. Conclusion Dofetilide concentration-dependently increased the outward and inward Na+/Ca 2+ exchange current in ventricular myocytes of adult guinea pigs.

Objective To investigate the effect of propofol on myocardial injury induced by hepatic ischemia/reperfusion (I/R) in rats and the role of PI3K/Akt signaling pathway. MethodsOne hundred and two male SD rats weighing 250-280 g were randomly divided into 5 groups:Ⅰ sham operation group (group S, n =6), ⅡI/R group ( n = 30), Ⅲ propofol group (group P, n = 30), Ⅳ propofol + LY294002 group (group P+ LY, n =18), and Ⅴ propofol + dimethylsulfoxide group (group P+ DMSO, n = 18). Hepatic I/R was produced by occlusion of hepatic pedicle for 30 min followed by reperfusion in group Ⅱ - Ⅴ. Propofol 12 mg/kg, propofol 12mg/kg + LY294002 (a specific PI3K inhibitor) 1.5 mg/kg, and propofol 12 mg/kg + DMSO 0.5 ml were injected I.v.via femoral vein at 10 min before ischemia in group Ⅲ -Ⅴ respectively, and then propofol was infused I.v. At a rate of 30 mg· kg- 1 · h - 1 and the administration was stopped before the rats were sacrificed in group Ⅲ - Ⅴ . At 0,30, 60, 120, and 240 min of reperfusion (T1-5) in group Ⅱ and Ⅲ , and at T3.5 in group Ⅳ and Ⅴ , six rata were sacrificed and myocardial tissues were taken for determination of the total Akt (t-Akt) and phosphorylated Akt (p-Akt) expression and Bcl-2 expression and apoptosis were detected at T3. The hepatic tissues were taken for microscopic examination. The rats were sacrificed at T1 and the parameters mentioned above were detected in group Ⅰ . ResultsCompared with group Ⅰ , p-Akt expression and apoptosis rate were significantly increased in the other4 groups, and Bcl-2 expression was up-regulated in group Ⅱ , Ⅲ and Ⅴ (P ＜ 0.05). Compared with group Ⅱ , p-Akt and Bcl-2 expression was up-regulated, and the apoptosis rate was significantly decreased in group Ⅲand Ⅴ ( P ＜ 0.05). Compared with group Ⅲ , p-Akt and Bcl-2 expression was down-regulated, and the apoptosis rate was significantly increased in group Ⅳ ( P ＜ 0.05). The microscopic examination showed that the injury to the hepatic tissues was less severer in group Ⅲ and Ⅴ than in group Ⅱ and Ⅳ. ConclusionPropofol can attenuate myocardial injury induced by hepatic I/R in rats by activation of PI3K/Akt signaling pathway.

Aim This study aimed at investigating the postconditioning protective effect of KB-R7943 and the proper administration time on cardiac ischemia-reperfusion injury in isolated rat heart. Methods Rat heart was isolated quickly when the animal was anesthetized. With Langendorff perfusion, the left anterior descending coronary artery was ligated for 30 min, then released for 120 min in isolated rat heart. Left ventricular function (LVF) and the infarct size of left ventricle were determined. Result Compared with control, KB-R7943 at 1 ?mol?L-1 perfused during the early period of the reperfusion prevented the post-ischemic depression of LVF, decreased the infarct size by 77 %(P