摘要
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。
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. GroupⅠ control group; GroupⅡ with drugs given before ischemia phase(divided into 3 groups: FDPⅠ, DXMⅠ and FDPⅠ+ DXMⅠ); GroupⅢ 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 FDPⅠ and DXMⅠ than in FDPⅡ and even slower in FDP group than in DXM group; CK and cTnI levels rose slower in FDPⅠ+DXMⅠ than in FDPⅠ and DXMⅠ.Conclusion FDP given during ischemia and DXM could effectively protect the myocardium from reperfusion injury following hemorrhagic shock.
出处
《中国危重病急救医学》
CAS
CSCD
2004年第1期29-32,共4页
Chinese Critical Care Medicine
基金
安徽省高等学校青年教师科研计划项目 (2 0 0 2 jq161)
