1,6-二磷酸果糖和地塞米松对家兔失血性休克缺血-再灌注损伤的影响

目的　在家兔失血性休克模型上 ,探讨心肌缺血再灌注损伤机制 ,比较 1,6二磷酸果糖(FDP)和地塞米松 (DXM)对心肌缺血再灌注的保护作用。方法　按照 Wiggers改良法制作兔失血性休克模型。4 8只家兔随机分成 3组 : 组为对照组 ; 组为休克前给药组 (又分为 FDP 、DXM 及 FDP DXM 3组 ) ; 组为再灌注时给药组 (又分为 FDP 和 DXM 2组 )。观察血浆肌酸激酶 (CK)、心肌肌钙蛋白 I(c Tn I)含量及心肌细胞凋亡情况。结果　各组 CK、c Tn I基础值均无统计学差异 ;与对照组相比 , 组 CK、c Tn I及心肌细胞凋亡指数下降或明显下降 (P<0 .0 5或 P<0 .0 1) ; 组在休克时间点均无统计学意义 ,而再灌注时间点有下降或下降趋势 ,有统计学差异 (P<0 .0 5或 P<0 .0 1) ;与 FDP 和 DXM 组相比 ,FDP 和DXM 组的 CK和 c Tn I上升幅度均有减慢趋势 ,以 FDP组减慢趋势更加明显 ;休克给药组间比较 ,FDP DXM 组的 CK和 c Tn I上升幅度均减慢。结论　 FDP和 DXM对失血性休克引起的缺血再灌注损伤均有保护作用 ,但 FDP仅在缺血开绐给药才能充分发挥其效应 ,二者联合用药对心肌保护有更好的效果。

Effect of fructose-1,6-diphosphate and dexamethasone on ischemia/reperfusion injury after hemorrhagic shock in rabbits

OBJECTIVE: To investigate the mechanism of myocardial ischemia/reperfusion injury and the protective effect of fructose-1, 6-diphosphagic (FDP) and dexamethasone (DXM) in hemorrhagic shock in rabbits. METHODS: Using a hemorrhagic shock model of Wiggers, 48 rabbits were randomly divided into 6 groups. Group I control group; GroupII with drugs given before ischemia phase (divided into 3 groups: FDP I, DXM I and FDP I+ DXM I); Group III with drugs given in reperfusion phase (divided into 2 groups: FDPII and DXMII). The levels of creatine kinase (CK) and troponin I (cTnI) in plasma were measured, and myocyte apoptosis index was assessed. RESULTS: Baseline levels of CK and cTnI were similar in three groups; CK and cTnI and apoptosis index were lower or with a lower tendency in groupII and in groupIII (P<0.05 or P<0.01); CK and cTnI showed a lower tendency in rise in FDP I and DXM I than in FDPII and even slower in FDP group than in DXM group; CK and cTnI levels rose slower in FDP I+DXM I than in FDP I and DXM I. CONCLUSION: FDP given during ischemia and DXM could effectively protect the myocardium from reperfusion injury following hemorrhagic shock.