| After the attact of myocardiac infarction, the ischemic myocardium get the blood reperfusion rapidly by the intravenous thrombolytic therapy, percutaneous transcluminal coronary angioplasty ( PTCA ) and the thrombolytic therapy of coronary artery clinically. Therefore, it may decrease the injury of cells and inhibit the extant of myocardium necrosis, which survive the myocardial tissue and cells. But during the processes of myocardial ischemic and injury, it can't recover the function of tissue and organ while exacerbate the function and structure injury after ischemic myocardium reperfussion due to the cell ischemic and producing the metabolic disorder. The phenomenoen is called for ischemic-reperfusion injury. Although the pathogenic mechanism of ischemic -refusion injury is not clarified thorough. Generally it is thorough that the final pathway of myocardium ischemic-refusion injury is the overload of calcium at the time of reperfusion. The calcium antagonist can block the calcium ion entering intracellular by calcium channel and tracellular calcureous releasing, reduce the concentration and utilization ratio of intrcellular free calcium,inhibit the activity of ATP-ase, decrease the decompose of ATP, lower the myocardium heaping up of abnormal sustance. and has the function of agains ischemic-refusion. Pranidipine is a new kind of langacting calcium antagonist belonging to Fluazifop. It's half life in plasm is about 30 hours and can maintain it concentration in blood stably. At present, the study reports on this drug are very little, so in this experiment by observing the effects of Pranidipin on the cardiac function of isolatd rat hearts underwent ischemic-refusion , author wants to determine whether Pranidipine is of protect function against cardiac ischemic-refusion in order to give some reliable experiment evidence.Materials and Methods1. drugs and animals Pranidipine is from Japanese otuka seiyaku Co. and other reagent is the analysis reagent sell publicly. Wistar Rat is from the Animal Center of China Medical University.2. Animal model 40 Wistar Rats in good health and weight among 230 - 260 g, anesthetized by enterocoelia injection of pentobarbital ( 60 mg/kg ) accept cardiac extirpation after being injected lOOUheparin through right femoral vein. The hearts are put in 4(€ solution of Krebs-Heinseleit ( KH) rapidly and hung on the Langendorff device after retrograde intubation of aorta subsequently. In the condition of perfusion of 37℃ and 75mmHg KH solution which is oxygenated by 95% O2 and 5% CO2 adequately, insert the water infusing tract into the left ventricle, infuse water about 0. 2 -0.4 ml, make the di-astolic pressure of left ventricle to 8mmHg, pace the heart at 360 b/ min by a pacing electrode which is inserted in right atrium, record the EGG, left ventricle pressure ( using the Japanese NEC 360 multi-leadphysio-recorder) , and the infusion volume ( America 1206 blood-flow measuring equipment) , and begin the experiment when the left ventricle pressure and infusion volume are stable in 10 minutes.3. experiment methods and groups The experiment is divided into two parts. First is to determine the effects of cardiac function and coronary artery dilatation of the unischemis hearts in different drug concentration. The rats are divided into 2 groups and 8 rats in each group. In comparing group, infusion of KH is in every stage; and in drug group, the concentration of infused drug is 0. 1 nmol/L,lnmol/ L,10nmol/L,100nmol/L differently. Each group is paced at 360 b/ min during the experiment, change the drug concentration every 10 minutes after 5 minutes of the experiment beginning, and observe the changing of different index. Make 24 rats into 3 groups, use drug for about 10 minutes after 5minutes of the experiment beginning, make 25 minutes of thorough ischemia and 30 minutes reperfusion and observe the changing of different index. Soak the ischemic hearts unpaced in the 37℃ KH solution, and divided into comparing group, 1nmol/L pranidipine...
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