The Research On The Mechanism Of Myoblast Transplant Therapy For Ischemic Heart Disease

In the mature individual, the myocardium belongs to the ultimate differentiated cell. It can be replaced by the scar tissue in case it is damaged. At present the therapies for the myocardial damage including thrombolysis and CABG (coronary artery bypass graft) etc. can only recover reperfusion, and cannot repair or reverse the necrosed myocardium. Infarct causes that myocardial cells, which possesses contractive function, decrease evidently and leads to the congestive heart failure finally. Recently, the research on applying skeletal muscle myoblast to transplant within the myocardium to replace the damaged myocardium and scar tissue developed greatly and are widely paid attention to.34 healthy adult Zelanian rabbits are used in this experiment. Establish the models of myocardial ischemic damage established by ligating the left anterior descending branch of the coronary artery. The autologous skeletal muscle myoblast are cultured and amplified in vitro and are marked with BrdU, (3.5-5) ×107cells are transplanted into the area of the autologous acute myocardial infarct. In the control group, the autologous endothelial cells and skeletal muscle cells are transplanted intothe area of acute myocardial infarct. 2, 4 and 8 weeks later, physical, histological and cytological examination were conducted to observe the influence of the satellite transplantatation cell on the myocardial coma and the stunned myocardium and the system of improving the function of the heart.Experimental Result: The myoblast and muscle fiber with fluorescence are observed in the infarct area and part of them have already been differentiated into striated muscle. It is showed that the section area and volume of the normal myocardial cell increased and turned out to be hypertrophic as time passed since infarct.The myoblast transplant therapy for ischemic heart disease does improve the contractive function of the ventricle.After the transplantation of the myoblast, the part recovery of function of the stunned and hibernating myocardial cell in the infarct focus can be accelerated. Thus the heart function can be improved. This may be the main reason of improving heart function.In the early stage, there is no evident difference in the local capillary network in the group of the skeletal muscle cell transplantation after the transplantation of the myoblast compared to the control group and non-therapy group. However, 8 weeks later, it increases apparently. Reestablishing the local microvessel network and improving the local microcirculation may be the part reason of improving the heart function.The myoblast, new-born blood capillary, and new-born fibroblast are interlaced like reticulation. It can accelerate the contract of the scar tissue; cause the strengthening of the left ventricle wall and the decrease of the volume, macroaxis, and occipitofrontal diameter of left ventricle in the late stage of transplantation. This may be the part reason of the rise the EF value of the left ventricle after infarct.It is showed in the experiment that 1. it is discovered that no connection can be established between the myoblast and the myocardial cell. Thus the functional plasmodium can be formed. That the myoblast attend contraction passively is not the reason of improving the heart function compared to the group of the skeletal muscle cell transplantation. 2. After the transplantation of the myoblast, the part recovery of function of the stunned and hibernating myocardial cell in the infarct focus can be accelerated. Thus the heart function can be improved. 3. The adjustment and control of the connection between the myocardial cell and the myoblast are required to be researched further. To make the cell attend the work of the cell actually is the ultimate objective of the cellular tissue project.