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首页> 外文期刊>American Journal of Physiology >Evolution of scar structure, mechanics, and ventricular function after myocardial infarction in the rat.
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Evolution of scar structure, mechanics, and ventricular function after myocardial infarction in the rat.

机译:大鼠心肌梗死后瘢痕结构,力学和心室功能的演变。

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摘要

The mechanical properties of the healing scar are an important determinant of heart function following myocardial infarction. Yet the relationship between scar structure, scar mechanics, and ventricular function remains poorly understood, in part because no published study has tracked all of these factors simultaneously in any animal model. We therefore studied the temporal evolution of scar structure, scar mechanics, and left ventricular (LV) function in large anterior myocardial infarcts in rats. At 1, 2, 3, and 6 wk after left anterior descending coronary ligation, we examined LV function using sonomicrometry, infarct mechanical properties using biaxial mechanical testing, infarct structure using polarized light microscopy, and scar collagen content and cross-linking using biochemical assays. Healing infarcts in the rat were structurally and mechanically isotropic at all time points. Collagen content increased with time and was the primary determinant of scar mechanical properties. The presence of healing infarcts influenced systolic LV function through a rightward shift of the end-systolic pressure-volume relationship (ESPVR) that depended on infarct size, infarct collagen content, and LV dilation. We conclude that in sharp contrast to previous reports in large animal models, healing infarcts are structurally and mechanically isotropic in the standard rat model of myocardial infarction. On the basis of the regional strain patterns we observed in healing rat infarcts in this study and in healing pig infarcts in previous studies, we hypothesize that the local pattern of stretching determines collagen alignment in healing myocardial infarct scars.
机译:疤痕愈合的机械特性是心肌梗死后心脏功能的重要决定因素。然而,疤痕结构,疤痕力学和心室功能之间的关系仍然知之甚少,部分原因是没有任何发表的研究在任何动物模型中同时追踪所有这些因素。因此,我们研究了大鼠大面积前心肌梗塞的瘢痕结构,瘢痕力学和左心室(LV)功能的时间演变。在左前降支结扎后第1、2、3和6周,我们使用体测法检查了LV功能,使用双轴机械测试检查了梗塞的机械性能,使用了偏光显微镜检查了梗塞的结构,并使用生化分析检查了疤痕胶原含量和交联。在所有时间点,大鼠的治疗性梗塞在结构和机械上都是各向同性的。胶原蛋白含量随时间增加,是疤痕机械性能的主要决定因素。梗塞的愈合通过收缩末期压力-容积关系(ESPVR)的右移而影响收缩期LV功能,收缩末期压力-体积关系(ESPVR)取决于梗死面积,梗死胶原蛋白含量和LV扩张。我们得出结论,与先前在大型动物模型中的报道形成鲜明对比的是,在标准的心肌梗死大鼠模型中,治疗性梗死在结构和机械上各向同性。基于我们在本研究中治愈的大鼠梗塞和先前研究中的愈合猪梗塞中观察到的区域应变模式,我们假设拉伸的局部模式决定了愈合的心肌梗塞疤痕中的胶原蛋白排列。

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