果糖二磷酸钾盐抗缺血再灌注心律失常作用的实验研究

目的:探讨果糖二磷酸钾盐(FDPK)的抗心肌缺血再灌注心律失常作用及其机制。方法:取大鼠60只,随机分为模型对照组,FDPK大、中、小剂量组(80、40、20mg·kg-1),1,6-二磷酸果糖(FDP)组、氯化钾组共6组,采用冠脉结扎、松扎法建立心肌缺血再灌注心律失常模型,观察各组心律失常评分、心肌组织中超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量和三磷酸腺苷(ATP)酶的活性;此外,建立兔低钾血症模型,分别给予生理盐水、氯化钾、门冬氨酸钾镁和FDPK,检测各组细胞内钾离子浓度。结果:与模型对照组比较,FDPK(80、40mg·kg-1)能降低心律失常评分、升高SOD和ATP酶活性、降低MDA含量(P<0.01或P<0.05),并优于FDP组和氯化钾组;与给予生理盐水相比,FDPK能明显增加兔细胞内钾离子浓度(P<0.01)。结论:FDPK具有抗缺血再灌注心律失常作用,其作用机制可能与抗氧自由基产生和促进钾离子进入细胞有关。

Experimental Study on the Effects of Potassium Fructose Diphosphate on Ischemia-reperfusion Induced Arrhythmia

OBJECTIVE： To investigate the effect of potassium fructose diphosphate （FDPK） on ischemia-reperfusion induced by arrhythmia and its mechanism.METHODS： 60 rats were randomized into model group,FDPK high-dose group （80 mg·kg-1）,FDPK medium-dose group （40 mg·kg-1）,FDPK low-dose group （20 mg·kg-1）,FDP group and potassium chloride （KCl） group.Ischemia-reperfusion induced by arrhythmia model was induced by occlusion and reirregation.The score of arrhythmia,the level of MDA,the activity of SOD and ATPnase of those groups were investigated.Hypokalemia rabbit model was induced and treated with normal saline,KCl,magnesium aspartate and FDPK.The concentrations of potassium ion in lymphocyte were also detected.RESULTS： As compared with model group,FDPK could decrease the score of arrhythmia,the level of MDA but increase the activity of SOD and ATPnase （P0.01 or P0.05）.Above index of FDPK groups was superior to that of FDP group and KCl group.FDPK could increase the concentration of potassium ion,compared with normal saline （P0.01）.CONCLUSION： FDPK has sound effect on ischemia-reperfusion induced arrhythmia,which may be associated with the proliferation of antioxidant free radicals and acceleration of potassium ion across cell membrane.