| Arrhythmia is that the abnormal rhythm of heart cauced by the abnormality of trigger or conduction in myocardial.lt is characterized by the slow, fast, irregular or disordered palpitation, Its mainly forms are tachycardia, bradycardia, premature contraction, flutter and fibillation of ventricular or atrium, and atrio- ventricular block and so on.The myocardial ischemia reperfusion injury(IRI) is a dominant interference in the resuscitation therapy for acute myocardial infarction.lt expresses mainly arrhythmia.T5he mechanism is still not very clear, but it is generally accepted to be initially caused by the disturbance of energy metabolism, oxygen freeradicals and [Ca2+]i overloading. It is reported that frustose-1 , 6-diphosphate(FDP) is a significant intracellular metabolite which plays a direct role in regulating many metabolic pathways.FDP can improve myocardial function, protect against ischemia reperfusion, and reduce the occurrence rate of arrhythmia induced by ischemia-reperfusion by restoring and enhancing energy metabolic processes, and stabilizing the cell membrane, and inhibiting the generation of oxygen free radicals, anddecreasing the [Ca2+]i overloading. It has been shown that magnesium is activator that regulates all enzymatic reactions and the natural calcium-channel blocking. Moreover, magnesium plays an important role in the electrophysiology of heart, and reduce the damage of oxygen free radicals.Therefore working on the premise, it is speculated that fructose diphosphate magnesium (FDPM) which is substituted magnesium iron for sodium in fructose-1, 6-diphosphate may take a synergetic effect to protect the myocardial ischemia reperfusion injury and lower the occurrence of arrhythmia.This experiment mainly study the benefical effects of FDPM on myocardial arrhythmia induced by ischemia reperfusion injury and their mechanisms in rats.Is there the benefical effects of FDPM on myocardial arrhythmia induced by ischemia reperfusion injury superior to FDP or magnesium sulfate? The mechanism of protection is unknow.It remains a matter for further investigation.Objective: To study the protective effects of FDPM on the myocardial arrhythmia induced by ischemia reperfusion injury in rats, and observe electrocardiograph and hemodynamics, and the myocardial enzymology, and explore the protection of myocardial arrhythmia. To explain the mechanism of effects of FDPM on the arrhythmia induced by ischemia reperfusion injury in rats.Methods: Sixty Wistar rats were randomly divided into six groups: normal saline control group, large dose of FDPM treated group, middle dose of FDPM treated group, small dose of FDPM treated group, FDP treated group and magnesium sulfate treated group.The models were made by drawing then releaseing the suture advanced around the left coronary artery in rats.At the different time of ischemia and reperfusion in myocardium, the changes of electrocardiograph and hemodynamics were monitored, the specimens of heart and serum were determined.Results: (1) The therapy effects of FDPM increased +dp/dtmax, -dp/dtmax, vce-5kPa, Vpm, and decreased LVEDP and heart rate(HR).The effects of FDPM was mostly superior to FDP and magnesium sulfate.These results indicate that FDPM can improve hemodynamic parameters in the arrhythmia induced by ischemia reperfusion injury. (2 ) FDPM lowered the activity of creatine phosphokinase(CK) and lactic dehydrogenase(LDH) in serum and myocardium, reduced the occurrence rate of arrhythmia. Theeffects of FDPM was markedly superior to FDP and magnesium sulfate. These results indicate that FDPM have the protective effect on ischemia reperfusion injury and arrhythmia in myocardium. (3) FDPM increased the activity of Na+-K+-ATPase, Ca2+-ATPase, Mg2+-ATPase and superoxide dismutase (SOD) in myocardium, and reduced the content of lipid peroxidation (malondiadehyde, MDA)in myocardium.The results indicate that the mechanism of the therapy effects of FDPM are related to restore and enhance energy metabolism and improve the activity of... |