| Background and Objective: Regeneration is an essential function of the human body. Cardiomyocytes are thought to be terminally differentiated cells for their inability to regenerate and replace damaged myocardium. However, recent researches show that even in normal physiological situations, there exists the death of cardiomyocytes in hearts. When myocardial infarction happens, besides the acute death of cells caused by the lack of blood and oxygen and the exhaustion of energy metabolism, there exists apoptosis of cardiomyocytes at the same time. The cardiomyocytes have diminished dramatically when the myocardial infarction happens; meanwhile a rapid loss of cardiac mass would occur even when a very low apoptosis level of cardiomyocytes exists. This indicates that the diseased heart could not continue to function if it depends on the cardiac hypertrophy and in the absence of new myocyte formation. We did experiments on rats to evaluate the ventricular haemodynamics after myocardial infarction, the histological and ultrastructural change of cardiomyocytes, the apoptosis level of cardiomyocytes, the process of proliferation and the cell cycle, the expression of the proteins related to the cell cycle and the activity of telomerase, in order to study the consequences of the proliferation and differentiation of cardiomyocytes in ventricular dilation and wall restructuring after infarction and the possible regulating mechanism.Methods: Rats' myocardial infarction (MI) models were mimicked by ligation of the left coronary artery. We used the hematoxylin-eosin stain to assess the infarct size and the change of the cardiac structure after infarction. The cardiac function was evaluated by the physiological signal recording system (Part I) . The apoptosis level was examined by the flow cytometry (Part II) . Immunofluorescence microscopy was used to examine the change of the myocyte mitotic index and the variation of a-sarcomeric actin (Part III) ; electron microscope was used to observe the cardiac ultrastructure (Part IV) ; With the method of flow cytometry, the cell cycle was examined. By using the immunohistochemical analysis,we examined the p27, cyclin D2, Cdk4 (Part V) . Southern blot analysis was used to observe the average length of the telomere fragments, the telomerase expression was also observed by the immunohistochemical analysis (Part VI) .Results: Part I: The cardiac function declined after MI. Compared with the sham group, LVSP and dp/dt declined significantly but LVEDP kept rising. Histological analysis showed that the cardiomyocytes necrosis was most palpable within the first three days after MI, and the swelling of cardiomyocytes and the pervasion of inflamed cells were gradually obvious in these days, the myofibers were arrayed out of order or broken up in part of the myocardium, where the karyopycnosis and karyoklasis can be found. After 14 days, myocardium hypertrophy can be detected, in which the myofiber were dispersed and macrophage infiltrated. After 30 days, the fibroblast activation was observed in the infarction area, the myocardium hypertrophy and nucleus enlargement were observed also;Part II: The apoptosis level was 2.71-fold, 4.45-fold, 5.81-fold, 10.24-fold and 9.89-fold higher at 1day, 3 days, 7days, 14 days and 30 days after MI than in the sham group, respectively;Part III: The myocyte mitotic index were 1.24-fold, 2.00-fold, 2.23-fold, 2.20-fold and 1.89-fold higher at lday, 3 days, 7days, 14 days and 30 days after MI than in the sham group, respectively; the a-sarcomeric actin expression in the non-infarction area was 1.12-fold, 1.25-fold and 1.23-fold higher at 7day, 14 days and 30 days after MI than in the sham group, respectively;Part IV: Electron micrograph indicated that the cardiomyocyte plasma membranes, mitochondrial membrane and the mitochondrial crista were integrated, the myofiber content was still trim, the nuclear membranes of the cardiomyocyte were complete. In some cardiomyocytes the reduction of myofiber could be found, the nucleus enlarged, nucleoli became obv...
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