【摘要】 目的探讨心力衰竭(简称心衰)犬心房组织基质金属蛋白酶-2(MMP-2)及其组织抑制因子1、2(TIMP-1、2)的基因表达及其与心房扩大及心房颤动(简称房颤)发生维持的关系。方法选健康成年杂种犬14只随机分为心室快速起搏致心衰组和对照组,采用Burst刺激诱发房颤,逆转录-聚合酶链式反应技术和免疫组化方法检测两组左右心房组织MMP-2和TIMP-1、2的mRNA和蛋白表达,采集心房标本前超声心动图测定左右心房收缩末期面积。结果心衰组左室射血分数下降、房颤的诱发和维持时间增加,左右心房均扩大。MMP-2的mRNA和蛋白表达在左右心房中均上调;TIMP-2的mRNA在左右心房中无明显改变,但MMP-2/TIMP-2的mRNA和蛋白的比值在左右心房中均升高(P<0.01);TIMP-1的mRNA和蛋白表达在左右心房中均下调。心衰组,房颤持续时间与左房面积呈正相关。结论心房组织MMP-2和TIMP-1、2的基因表达改变以及MMP-2/TIMP-2表达失衡可能是心衰时心房扩大及房颤发生与维持的分子机制之一。更多还原

【Abstract】 Objective To study the relationship between gene expression of MMP-2 and TIMP-1,2 with atrial enlargement and atrial fibrillation(AF) during heart failure(HF). Methods 14 mongrel dogs were randomized into HF induced by ventricular tachypacing and control group. Burst atrial pacing was used to induce AF. And the mRNA and protein level of MMP-2 and TIMP-1,2 were detected by reverse transcription-polymerase chain reaction and immunohistochemical technique. Atrial systolic area were measured by transthoracic echocardiography before atrial specimen been collected. Results Compared with control group, left ventricular ejection fraction decreased , The inducible rate and sustained time of AF increased in HF group;atrial size of HF group was markedly greater than the controls.The mRNA and protein level of MMP-2 increased evidently in both left atrial(LA) and right atrial (RA), TIMP-2 mRNA decreased in LA and had no change in RA and its protein had no change in both atrium,whereas the ratio of MMP-2/TIMP-2 of mRNA and protein increased markedly in both LA and RA of HF group. Both mRNA and protein level of TIMP-1 decreased significantly in both LA and RA of HF group. The lasting time of AF has a positive correlation with area of LA during HF(r=0.806,P=0.029). Conclusions The changes of MMP-2 and TIMP-1,2 gene expression and the unbalance of MMP-2/TIMP-2 appear to be a molecular mechanism of atrial enlagement and AF during HF.更多还原