CAJ | 학술논문

心力衰竭时心功能进行性恶化，其机制尚未阐明。用冠脉内微栓造成羊慢性心力衰竭(CHF)模型，起搏诱导兔CHF模型及慢性输注去甲肾上腺素雪豹模型，研究了CHF时心肌细胞凋亡。CHF早期羊心肌细胞凋亡的超微结构特征为核染色质聚集成团，并向核膜方向移动，而肌质网和细胞器完整。凋亡的心肌细胞数量明显增加。起搏诱导兔CHF时，血浆去甲肾上腺素水平增高，心肌细胞凋亡发生。慢性输注去甲肾上腺素时，心肌细胞凋亡增加，伴凋亡蛋白BAX表达增加。结果提示，CHF时心肌细胞凋亡发生，去甲肾上腺素诱导心肌细胞凋亡。心功能的进行性恶化与之有关。进一步阐明心肌细胞凋亡的信号通路，将为CHF 的预防和治疗提供新的途径。
심력쇠갈시심공능진행성악화，기궤제상미천명。용관맥 내미전조성양만성 심력쇠갈(CHF)모형，기박유도토CHF모형급만성수주거갑신상선소설표모형，연구료CHF시 심기세포조망。CHF조기양심기세포조망적초미결구특정위핵염색질취집성단，병향핵막방 향이동，이기질망화세포기완정。조망적심기세포수량명현증가。기박유도토CHF시，혈 장 거갑신상선소수평증고，심기세포조망발생。만성수주거갑신상선소시，심기세포조망증가 ，반조망단백BAX표체증가。결과제시，CHF시심기세포조망발생，거갑신상선소유도심기 세포조망。심공능적진행성악화여지유관。진일보천명심기세포조망적신호통로，장위CHF 적예방화치료제공신적도경。
The progressive worsening of heart function is a characteristic feature of the h eart failure state. The mechanisms responsible for the process remain unclear. T o determine whether cardiomyocyte apoptosis occurred in chronic heart failure (CHF), and whether norepinephrine (NE) produce d cardiomyocyte apoptosis, the study in coronary embolization-in duced sheep heart failure, pacing-induced rabbit heart failure, as well as NE-infusion ferrets was carried out. Apoptosis was detected by electron microscopy, terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL), and a mo noclonal antibody against single stranded DNA (Mab) staining. The expression of apoptotic protein Bax was measured by Western blot analysis. The results showed that the ultrastructural features of c ardiomyocyte apoptosis, including margination and compaction of nuclear chromatin, were identified in th e failed sheep heart. In these cells, the sarcolemma and the inner organells were intact. TUNEL positive nuclei were increased in the failed sheep heart. Mab positive nuclei were increased in pacing-induced rabbi t heart failure accompanied by an increase of plasma NE. NE infusion increased the number of TUNEL positive nuclei and the expression of Bax protein. The results suggest that cardiomyocyte apoptosis occu rs in CHF and NE produces cardiomyocyte apoptosis. NE-exerted apoptosis may contribute to the progression of CHF. Further elucidation of the signal pathway leading to cardiomyocyte apopt osis may open new routes to prevention and treatment of CHF.