Improved Myoardial Protection by Addition of Fructose-1.6-diphosphate to Crystalloid Cardioplegic Solution in the Isolated Working Rat Heart

흰쥐의 적출 작업성 심장에서 허혈성 심정지시 Fructose-1.6-diphosphate(FDP)의 심근보호 작용

Currently numerous methods are in use for myocardial protection from the ravages of ischemia and hypoxia. This study was designed to compare with FDP-GIK[Group II, n=8] and GIK cardioplegic solution[Group I, n=8] in ability of myocardial protection and was examined in the isolated working rat heart subjected to long period[120 min] of hypothermic[10 - 15K] ischemic arrest with multidose[every 30 min] cardioplegic infusion. During postischemic reperfusion period 20 min, hemodynamic functions[aortic flow, coronary flow, peak aortic pressure, cardiac output, heart rate], biochemical enzymatic & electrical activities were evaluated. The time from onset of reperfusion to the return of regular sinus rhythm was significantly reduced from 87$\pm$3 sec to 17$\pm$2 sec[P<0.05]. The postischemic recovery of aortic flow was better in the group II [95.1$\pm$3.3% of its preischemic control level] than in the Group I [75.4$\pm$6.8%] [P<0.05]. Cardiac output and stroke volume was also better in the group[91.3$\pm$1.6%, 89.4$\pm$2.6%, respectively] than in the Group I [79.1$\pm$3.7%, 77.0$\pm$4.8%, respectively] [P<0. 05]. Creatine kinase leakage was also significantly reduced from 33.8$\pm$4.9 IU /10 min / gm * dry weight to 15.4$\pm$3.6 IU /10 min /gm * dry weight[P<0.05]. It is suggested that adding FDP to GIK cardioplegic solution improves its ability to protect the heart against long period of hypoxic ischemia.