| [Objective] To study the effect of cardiomytocyte apoptosis in the cardiac remodeling and the regulation of apoptosis during chronic pressure overload. [Methods] The models of chronic pressure overload-induced heart failure were made with rabbits. We investigated the dynamic changes of myocyte apoptosis and the expression of bcl-2 -. bax and Fas protein in ventricle and atrium of chronic pressure overload, using in situ terminal deoxynucleotidyl transferase mediated dUTP nick end labeling(TUNEL) and strept avidin- biotin-enzyme complex(SABC) immunohitochemistry. [Result] 1... During chronic pressure overload, cardiac cellular hypertrophy occurred in left ventricular and left atria with day 14 group and heart failure(HF) group, and in right ventricular with HF group. 2~. The number of cardiomyocyte apoptosis in left ventricular was increased after operation, the most was in HF group. There number of day 3 group was higher than the number of day 7 group. The number of apoptosis cell in left atria and right ventricular was lighted increased in day 3 group, and were increased obviously in HF group. 3-. The number of expression bcl-2 protein of myocyte, in left ventricular was increased after operation, the most was in HF group; and in left atria and right ventricular was lighted increased in day 3 group, and were increased obviously in HF group. The number of expression bax protein of myocyte, in left ventricular were increased in day 1 group and HF froup; in left atria and right ventricular were only increased in HF group. And the expression Fas protein of myocyte were in left ventricular, right ventricular and left atria with HF group. [Conclution] 1 During chronic pressure overload, the cardiac remodling of atrium and ventriculars were appeared step by step. 2-. During chronic pressure overload, the peak of myocyte apoptosis by far preceded the peak of myocyte hypertrophy. Different phases had different cause which occurred myocyte apoptosis. Pressure load was the inducement of myocyte apoptosis, and the myocyte paoptosis was one of the mechanism of cardiac remodeling. 3 During chronic pressure overload, the elevation of bcl-2 protein could restrain the effect of bax and Fas protein. The broken body balance may be the inducement of bax protein expression. The expression of Fas protein was only in heart failure. -3-... |
