CAJ | 학술논문

Objective To investigate the effect and significance of cardiomyocyte apoptosis and cardiomyocyte proliferation on cardiac hypertrophy by observing the dynamic changes of them during the development of cardiac hypertrophy in spontaneously hypertensive rats (SHR). Methods Hearts were excised from SHR and Wistar-Kyoto rats(WKY) at different ages. Cardiac hypertrophic index (CHI) was calculated as the radio of heart weight to body weight; Cardiomyocyte apoptosis was identified by in situ TDT-mediated dUTP nick end labeling (TUNEL); Localization and expression of proliferating cell nuclear antigen (PCNA) were examined by immunohistochemistry. Results Compared with age-matched WKY, CHI in SHR was significantly increased at 12 weeks old and 24 weeks old (3. 604 ± 0. 089 vs 2. 997 ± 0. 166, P＜0.01; 4. 156 ± 0. 385 vs 3. 119 ± 0. 208, P ＜ 0. 01 ) ,and CHI in SHR was increased little by little with the age increasing and attained plaiform since 20 weeks old. In contrast with age-matched WKY, cardiomyocyte apoptotic index (APOI) in SHR at 12 weeks was not increased significantly (4. 248 ± 1. 592 vs 3. 678 ± 0. 856, P ＞ 0. 05 ), but decreased markedly when their age were 24 weeks (3. 207 ± 1. 794 vs 5. 494 ± 1. 372, P ＜0. 05); APOI in SHR at 12 weeks old, 16 weeks old, 20 weeks old and 24weeks old were 4. 248 ± 1. 592, 5. 707 ± 1. 322, 7. 436 ± 1. 128, 3. 207 ± 1. 794, respectively. On the other hand,APOI in SHR from 12 weeks old to 20 weeks old increased gradually, and attained peak at 20 weeks old, but decreased markedly after 20 weeks old ( P ＜0. 01 ). Compared with age-matched WKY, the rate of cardiomyocyte PCNA positive labeling (PCNAR) in SHR at 12 weeks old and 24 weeks old didn' t have obvious difference. Conclusion Imbalance of cardiomyocyte apoptosis and cardiomyocyte proliferation existed during the development of cardiac hypertrophy in spontaneously hypertensive rats.