1，6—二磷酸果糖预处理对离体大鼠心肌缺血再灌注损伤的保护作用

目的:观察1,6-二磷酸果糖(FDP)预处理对离体大鼠心肌缺血再灌注损伤的保护作用。方法:随机分成两组应用Iangendorff灌注装置用Krehs-Ring(K-R)液和K-R液加FDP5mmol·L~(1)对大鼠心脏进行缺血前预处理10分钟,缺血20分钟和再灌注20分钟实验,观察每期左室舒张未期压(LVEDP)、心肌组织内二醛(MDA)含量、超氧歧化物酶(SOD)的活性。Wistar大鼠心脏48个,每8个一组进行对照组和FDP组对比观察。结果:在缺血前期FDP组LVEDP和MDA无明显差异,缺血期FDP组MDA变化与对照组比较明显下降(P<0.01),再灌注期FDP组LVEDP和MDA明显下降(P<0.05),在FDP组SOD活性明显增高(P<0.01)。结论:FDP预处理具有提高大鼠心肌耐缺氧力,对大鼠心肌缺血再灌注损伤具有保护作用,该保护作用的机制可能与清除氧自由基功能有关。

Protective effect of the fructose 1, 6-diphosphate preconditioning in the isolated rat hearts ischemia reperfusion model

Objective:To study the protective effect of the fructose 1,6-diphosphate preconditioning in the isolated rat hearts ischemia reperfusion model. Methods: The experiments were carried out in the isolated rat hearts ischemia reperfusion model. Aftre 10 min preperfusion with Krebs-Ringer(with and without 5mmol L-1 FDF) bicarbonate buffe(pH7.3), ischemia period 20 min followed by 20 min reperfusion with K-R buffer (with and without 5 mmol L-1 EDP). At the end of each step (preperfusion ischemia rcperfusion)the LVEDPand the concentrations of MDA SOD were determined on ventricle homogenates from 48 hearts(8 hearts for each period both for control and FDP preconditioning hearts). Results: FDF preconditioning could obviously decrease LVRDF and MDA during reperfusion(F<0.05), during ischemia(F<0.01), increase SOD versus control (P<0.01). Conclusion: FDP preconditioning might enhance the effect of root myocardium to hypoxia and have protective effect on ischemia reperfusion injury of rat myocardium. The mechamism of protective effect might be related to its free radical scavenging activty.