Abstract

To confirm whether there is myocytes proliferation in the adult rat with heart failure or not, and to investigate the relationship between myocyte proliferation and heart function. Descending anterior branch of left coronary artery was ligated in 20 adult male SD rats so as to establish an heart failure models. Eight rats were used as controls. Hemodynamic parameters, blood pressure (BP), left ventricle end systolic pressure (LVESP), left ventricle end diastolic pressure (LVEDP), +LVdp/dt(max), and -LVdp/dt(max), were measured 30 days after the coronary occlusion. Based on the results of heart function examination, the heart infarct rats were divided into 2 subgroups: cardiac functional compensation subgroup (8 rats), and cardiac functional decompensation subgroup (6 rats). Then the rats were killed and their hearts were taken out and stained with propidium iodide (PI) and antibody to alpha-sarcomeric actin. Immunohistochemistry was used to detect the proliferation cell nuclear antigen (PCNA). Confocal microscopy was used to observe the mitotic image. Light microscopy was used to observe the PCNA positive rate in the myocardium. (1) Mitotic images of myocytes could be identified by confocal microscopy in the left ventricle of all rats. (2) PCNA expression was detected in the nuclei of both infarct and normal hearts. The PCNA positive rate of the cardiac functional compensation subgroup was 7.2% +/- 1.4%, significantly higher than that of the control group (2.2% +/- 0.8%, P = 0.648). However, the PCNA positive rate of the cardiac functional decompensation subgroup was 3.0% +/- 1.3%, not significantly different from that of the control group (P = 0.648). (3) The correlation coefficient between PCNA-positivity of cardiomyocytes and +LVdp/dt(max) in the infarct rats were 0.80 (P < 0.01) and the correlation coefficient between PCNA-positivity of cardiomyocytes and -LVdp/dt(max) was -0.76 (P = 0.01). (1) There is myocyte proliferation in the adult rat heart. (2) Myocyte proliferation is positively correlated with heart systolic function, and negatively correlated with heart diastolic function in chronic heart failure.

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