摘要
目的 :探讨甲亢性心肌病的发病机制。方法 :建立甲亢性心肌病模型 ,观察心肌肥厚指数、心肌细胞直径、心肌胶原容积分数、心肌羟脯氨酸含量、超微结构改变、肌浆网钙泵 (myocardialsarco/endoplasmicCa2 + ATPase,SERCA)活力及心肌血管紧张素Ⅱ 1型受体 (angiotensinⅡreceptortype 1,AT1)mRNA表达的变化 ,以氯沙坦和福辛普利阻断肾素 血管紧张素系统 (renin angiotensinsystem ,RAS)的不同部位 ,观察RAS在甲亢性心肌病模型中的作用。结果 :L 甲状腺激素腹腔给药二周可致左右心室肌明显肥厚 ,胶原组织增生 ,肌浆网钙泵活力下降 ,AT1受体上调 ,氯沙坦和福辛普利可防止甲状腺素诱导的心肌肥厚形成。结论
Objective: To explore the etiology of hyperthyroid cardiomyopathy. Methods: We established a hyperthyroid cardiomyopathy model and measured cardiac hypertrophy index,cardiomyocyte diameter,collagen volume fraction ,hydroxyproline content,myocardial pathological changes,the activity of myocardial Sarco/Endoplasmic Ca 2+-ATPase(SERCA) and the level of angiotensin Ⅱreceptor type 1 (AT 1)mRNA expression in cardiac tissue;We determined the role of RAS in the development of thyroxine-incuced cardiac hypertrophy with losartan and fosinopril blocking different position of RAS. Results: In the rats treated by levothyroxine,the left and right ventricules were hypertrophic,collagen content was significantly higher,the activity of myocardial SERCA was clearly lower and an apparently higher level of AT 1 mRNA was seen than those in control rats. Losartan and fosinopril can both prevent the development of cardiac hypertrophy. Conclusion: RAS and SERCA play an important role in the development of hyperthyroid cardiomyopathy.
出处
《北京大学学报（医学版）》
CAS
CSCD
北大核心
2002年第4期337-341,共5页
Journal of Peking University:Health Sciences
关键词
甲亢性心肌病
肾素-血管紧张素系统
肌浆网钙泵
发病机制
心肌肥厚
Hyperthyroidism
Cardiomyopathy,hypertrophic
Renin-angiotensin system/physiopathol
Sarcoplasmic reticulum
Calcium pump
