心脏收缩力调节对慢性心力衰竭兔心肌重构的影响

发布时间：2018-12-14 15:47

【摘要】：目的:观察心脏收缩力调节(CCM)对慢性心力衰竭(心衰)兔心肌重构的影响并探讨其可能机制。方法:选取新西兰大白兔30只,分为假手术组、心衰组、心衰+CCM组,各组均n=10。假手术组仅开胸,未行升主动脉套扎。心衰组、心衰+CCM组通过升主动脉根部套扎法建立兔慢性心衰模型,心衰+CCM组模型制作成功后给予4周的CCM治疗。分别于实验第12周末和(或)第16周末对各组实验动物,采用超声心动图检测心脏功能,Masson染色评价心肌组织纤维化及病理形态改变,采用酶联免疫吸附法(ELISA)检测血浆B型利钠肽(BNP)水平,蛋白免疫印迹(Westernblot)法检测心肌组织I型胶原蛋白、Ⅲ型胶原蛋白、基质金属蛋白酶(MMP)2、MMP9、MMP抑制因子(TIMP)1、半乳糖凝集素3蛋白表达水平。结果:(1)超声心动图结果:实验第12周末与假手术组相比,心衰组、心衰+CCM组左心室收缩末内径(LVESD)、左心室舒张末内径(LVEDD)明显扩大,左心室缩短率(LVFS)和左心室射血分数(LVEF)明显下降(P0.05);实验第16周末,与心衰组相比,心衰+CCM组的LVESD、LVEDD、LVEF、LVFS指标明显改善(P0.05)。(2)病理学改变:Masson染色示与假手术组相比心衰组心肌组织胶原纤维含量明显增加(P0.05),CCM可部分减轻心衰心肌组织的胶原纤维沉积(P0.05)。(3)实验第12周末,与假手术组相比,心衰组、心衰+CCM组血浆BNP水平明显升高(P0.05)。实验第16周末,与心衰组相比,心衰+CCM组的血浆BNP水平下降,但仍高于假手术组(P0.05)。(4)Western blot法检测结果:心衰组心肌组织中I型胶原蛋白、Ⅲ型胶原蛋白、MMP2、MMP9、TIMP1、半乳糖凝集素3的蛋白表达水平明显高于假手术组(P0.05),心衰+CCM组心肌组织中I型胶原蛋白、Ⅲ型胶原蛋白、MMP2、MMP9、TIMP1、半乳糖凝集素3的蛋白表达水平较心衰组明显下降(P0.05),但仍高于假手术组(P0.05)。结论:心脏收缩力调节可以改善慢性心衰兔心功能及心肌重构,其机制可能与下调心衰心肌组织中I型胶原蛋白、Ⅲ型胶原蛋白、MMP2、MMP9、TIMP1、半乳糖凝集素3蛋白的表达有关。
[Abstract]:Aim: to investigate the effect of cardiac contractility on myocardial remodeling in rabbits with chronic heart failure (CHF) by regulating (CCM) and its possible mechanism. Methods: thirty New Zealand white rabbits were divided into sham operation group and heart failure CCM group. In the sham operation group, thoracotomy was only performed and no ascending aorta ligation was performed. Heart failure group, heart failure CCM group by ascending aortic root ligation method to establish a rabbit model of chronic heart failure, heart failure CCM model was successfully made 4 weeks after CCM treatment. Cardiac function was measured by echocardiography, and myocardial fibrosis and pathological changes were evaluated by Masson staining at the end of the 12th week and / or the 16th week of the experiment, respectively. The levels of B-type natriuretic peptide (BNP) in plasma were detected by enzyme-linked immunosorbent assay (ELISA), type I collagen, type 鈪，

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