心肌肥厚大鼠超声背向散射积分与细胞外基质重塑的相关性  

Myocardial Ultrasonic Backscatter in Cardiac Hypertrophy In Relation to Extracellular Matrix

作　　者：白江涛[1] 陆凤翔[1] 许迪[1] 陈莉[1] 周蕾[1] 雍永宏[1] 

机构地区：[1]南京医科大学第一附属医院心脏科,江苏南京210029

出　　处：《高血压杂志》2004年第6期527-532,共6页Chinese Journal of Hypertension

摘　　要：目的　探讨心肌肥厚大鼠背向散射积分的变化情况 ,并结合心肌细胞外基质的病理改变及其重要影响因子基质金属蛋白酶 (MMP 9)和其生理性抑制剂 (TIMP 1)在蛋白和基因水平的表达 ,探讨其相互关系。方法　SD大鼠腹腔注射去甲肾上腺素 ( 1 0 6mg/kg·d× 15d)建立心肌肥厚的动物模型 ,测定室间隔中部心肌的背向散射参数 ,并应用免疫组化和逆转录 -聚合酶链反应法 (RT PCR)方法检测心肌总体胶原、Ⅰ型和Ⅲ型胶原的改变 ,及MMP 9、TIMP 1蛋白和mRNA的表达 ,与超声测定的结果进行对比研究。结果　 ( 1)实验组大鼠心肌胶原成分及MMP 9、TIMP 1蛋白和mR NA的表达显著高于健康对照组 (P <0 0 1)。 ( 2 )超声背向散射积分 (IBS % )在实验组较对照组增高(P <0 0 1) ,与心肌胶原、MMP 9和TIMP 1蛋白和mRNA的表达之间存在相关性。结论　大鼠心肌肥厚时IBS %升高与胶原的过渡沉积密切相关 ,而MMP 9和TIMP 1可能是引起心肌细胞外基质重塑的重要机制之一。Objective To investigate the relations between myocardial ultrasonic integrated backscatter(IBS) and cardiac extracellular matrix(ECM) remodeling and expression of matrix metalloproteinase(MMP-9) as well as tissue inhibitor of metalloproteinase(TIMP-1) in rats with norepinephrine-induced cardiac hypertrophy. Methods The rat models was established by norepinephrine(NE 1.06 mg/kg·d) injectioned intraperitoneally twice a day for 15 days. Cardiac hypertrophy and extracellular matrix remodeling were evaluated by ultrasonic backscatter signal and morphological examination. The mRNA and protein expression of MMP-9 and TIMP-1 were examined by immunohistochemical and reverse transcription-polymerase chain reaction(RT-PCR) analysis. Results (1) The cardiac collagen and expression of MMP-9 and TIMP-1 were significantly increased in NE group compared with control( P < 0.01). (2)Myocardial integrated backscatter(IBS%)was increased in NE group, and was directly related to cardiac collagen, the mRNA and protein expression of MMP-9 and TIMP-1. Conclusion Myocardial ultrasonic integrated backscatter parameters was related with changes of extracellular matrix. MMP-9 and TIMP-1 play an important role in the cardiac ECM remodeling.

关 键 词：TIMP-1 心肌肥厚 MMP-9 大鼠 超声背向散射积分 表达 心肌细胞外基质 应法 结论 重塑 

分 类 号：R542.2[医药卫生—心血管疾病] R735[医药卫生—内科学]