摘要
目的 :研究 1.6-二磷酸果糖 ( FDP)对缺血再灌注心肌能量代谢和超微结构的影响 ,并探讨其作用机制。方法 :2 4只家兔随机平分为两组 ,1组 (体外循环组 12只 ) , 组 (体外循环 +1.6-二磷酸果糖组 12只 ) ,常规建立兔体外循环模型 ,用高效液相色谱法 ( HPLC)检测兔心肌缺血前后 ( ATP)含量的变化 ,并观察心肌超微结构的改变。结果 :缺血再灌注后 , 组心肌 ATP含量明显低于 组 ,分别是 1.65± 1.10 nmol/ g·心肌组织和 3 .91± 1.45 nmol/ g心肌组织 ,两组比较差异有极显著性 ( P<0 .0 1) ;心肌超微结构观察显示 , 组保存优于 组。结论 :FDP对缺血再灌注心肌能量代谢和超微结构有显著的保护作用。
Objective:This study compared the effects of fructose-1.6-disphosphate(FDP)on energy matabolism and ultrastructure of ischemia-reperfusion myocardium and investigated its mechanism.Methods:Twenty-four rabbits were divided randomly into two groups,group Ⅰ (cardiopulmonary bypass n=12),group Ⅱ (cardiopulmonary bypass+FDP n=12),the rabbit cardiopulmonary bypass model was set up,High-performance liquid chromatography (HPLC) was used to measure myocardial ATP,while myocardial ultrastructures were observed after reperfusion.Results:After reperfusion,the actives of ATP in group Ⅰ were obviously lower than in group Ⅱ ,1.65±1.10nmol/g myocardinm and 3.91±1.45nmol/g myocardinm (P<0.01);group Ⅱ was better than group Ⅰ in the protection of myocardial ultrastructures.Conclusions:FDP afford an excellent protection on energy matabolism and ultrastructures of ischemia-reperfusion myocardium. [
出处
《南通医学院学报》
2000年第1期30-31,共2页
ACTA Academiae Medicinae Nantong
关键词
心肌缺血
再灌注损伤
1.6-二磷酸果糖
能量代谢
myocardial ischemia
reperfusion injury
fructose-1.6-disphosphate(FDP)
glucolysis
ATP