果糖-1,6-二磷酸对急性冬眠心肌的保护作用

Protective Effect of Fructose 1,6 diphosphate on Acute Hibernating Myocardium

目的：观察果糖－１，６－二磷酸（ＦＤＰ）对急性冬眠心肌心功能和能量代谢的影响。方法：建立急性冬眠心肌模型，四道生理记录仪记录左心室内压力曲线、压力上升速率曲线；高效液相色谱法检测三磷酸腺苷及磷酸肌酸含量，蒽酮试剂检测心肌糖原含量，酶促偶联法测定灌流液中乳酸。结果：①冬眠９０分钟时，ＦＤＰ治疗组（ｎ＝７）心肌磷酸肌酸含量为３７．９１±２．９７μｍｏｌ／ｇ干重，明显高于冬眠组（ｎ＝７）的１５．７６±０．７６μｍｏｌ／ｇ干重（Ｐ＜０．０５）。②ＦＤＰ减少急性冬眠心肌舒张峰压上升幅度，在缺血３０分钟和６０分钟，ＦＤＰ治疗—再灌注组（ｎ＝６）明显低于冬眠—再灌注组（ｎ＝７，Ｐ＜０．０５）。冬眠期间，ＦＤＰ治疗—再灌注组左心室收缩峰压和左心室内压力最大上升速率均明显降低（Ｐ＜０．０５）。结论：ＦＤＰ可增加急性冬眠心肌的磷酸肌酸含量，改善心肌舒张功能，对冬眠心肌起一定的保护作用。

Objective:The effects of fructose 1,6 diphosphate(FDP) on heart function and myocardial energy metabolism in acute hibernating myocardium were evaluated. Methods:We set up an animal model of acute hibernating myocardium in isolated rat heart,which was perfused with human red blood cell enhanced KH buffer.Myocardial ATP,creatine phosphate (CrP),glycogen concentration and lactate uptake were measured. Results:In the FDP group( n =7),myocardial creatine phosphate was 37 91±2 97 μmol/g dry wt at 90 min of ischemia,and was much higher than that of the hibernating myocardium group( n=7,p<0 05). As compared with the hibernating myocardium—reperfusion group( n =7),left ventricular peak diastolic pressure (LVPDP) was reduced in FDP treated reperfusion group( n =6) at 30 and 60 min of ischemia ( p<0 05 ).FDP also decreased left ventricular peak systolic pressure (LVPSP) and the maximal rate of pressure rise(dp/dt max )during ischemia( p <0 05). Conclusions:The results suggest that FDP may be helpful to the acute hibernating myocardium by increasing the creatine phosphate content and improve the diastolic function.