Cardioprotective Effects Of The Studies Of Sodium Magnesium Fructose Diphosphate On Myocardium Undergong Ischemia-Reper Fusion And Their Mechanisms

The myocardial ischemia reperfusion injury (IRI)is a main interference in the reperfusion therapy for acute myocardial infarction.The mechanism is still not very clear ,but it is generlly accepted to be initially caused by the disturbance of energy metabolism,[Ca2+]i overloading and oxygen free radicals.lt has been shown that fructose- 1,6-diphosphate (FDP)improves myocardial function and protects against ischemia reperfusion injury by restoring and enhancing energy metabolic processes.As reported previously ,magnesium deficiency has led to myocardium energy metabolism disturbance and dysfunction as well as myocardial injury,whereas it is prevented and attenuated by magnesium,meanwhile magnesium loss accompanied by myocardial ischemia reperfusion may be also replenished.Working on the premise,it issepeculated that sodium magnesium fructose diphosphate(FDPM) which is in part substituted magnesium iron for sodium in fructose-1,6-diphosphate may take a synergetic effect to protect myocardial ischemia reperfusion ,thereby it can make more markedly effect to protect myocardial ischemia reperfusion injury .In the current study,the rats of myocardiac IRI in vivo,the isolated rat heart of myocardial IRI and cultured rat myocardial cells of hypoxia reoxygenation(HR) were used as models to investigate the protective effects of sodium magnesium fructose diphosphate on myocardial ischemia reperfusion and their mechanisms. The main results and conclusions were as follows:1.Sodium magnesium fructose diphosphate increased +dP/dtmax, -dP/dtmax in the rats suffered from acute myocardial ischemia reperfusion injury,decreased LVEDP and -dp/dtmax.The effect of FDPM was mostly superior to fructose-1,6-diphosphate and magnesium. These results indicate that FDPM can improve hemodynamic parameter.2.Sodium magnesium fructose diphosphate lowered creatinephosphokinase(CK) and lactic dehydrogenase (LDH) activity, decreased myocardial infarct size; the action of FDPM was markedly superior to fructose-1,6-diphosphate and magnesium sulfate. The results indicate that FDPM have the protective effect on myocardial ischemia reperfusion injury. 3. Sodium magnesium fructose diphosphate attenuated loss of ATP, ADPin myocardial infarction zone, thereby increased TAN and energycharge; improved the activity of Na+,K+-ATPase, Ca2+-ATPase , Mg2+-ATPase, superoxide dismutase (SOD) and reduced malondiadehyde (MDA) contents in myocardium. The results indicate that the mechanism of the protective effect of FDPM are related to restore and enhance energey metobolism and improve ATPase activity as well as be against oxygen free radicals.4. Sodium magnesium fructose diphosphate deduced the calciumcontents in myocardial infarction zone and [Ca2+] i of cultured rat myocardial cells.I The results indicate that the mechanism of the protective effect ofFDPM are related to decrease [Ca2+]i overloading.5. Sodium magnesium fructose diphosphate conduced to maintenance the integrality of myocardial cell ultrastructures.