首页> 外文期刊>Journal of Molecular and Cellular Cardiology >A comparative serial echocardiographic analysis of cardiac structure and function in rats subjected to pressure or volume overload.
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A comparative serial echocardiographic analysis of cardiac structure and function in rats subjected to pressure or volume overload.

机译:连续压力超声心动图分析的心脏结构和功能的大鼠承受压力或容量超负荷。

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Heart failure is a leading cause of death that is reaching epidemic proportions. It is a clinical syndrome attributable to a multitude of factors that begins with a compensatory response known as hypertrophy, followed by a decompensatory response that eventually results in failure. Heart failure can be triggered when the heart is subjected to extended periods of pathological pressure overload (PO) or volume overload (VO). To date there have been no comparative serial echocardiographic studies outlining the progression of hypertrophy in PO versus VO rats. We hypothesized that PO or VO would induce differential cardiac remodeling leading to contractile dysfunction with subsequent heart failure. To address this hypothesis we used echocardiography to study the serial progression of heart structure and function in rat models of both PO- and VO-induced hypertrophy. PO or VO were induced by performing abdominal aortic banding or aortocaval shunt procedures, respectively, while cardiac structure and function were assessed in both models by M-mode and Doppler echocardiography at key time intervals. PO rats showed progressive wall thickening consistent with concentric hypertrophy, while VO rats showed marked left ventricular dilatation consistent with eccentric hypertrophy. Systolic dysfunction occurred early in VO compared to PO. Diastolic dysfunction was evident in PO, while VO showed signs of enhanced diastolic function. PO and VO induced differential changes in cardiac structure and function during the progression of compensated hypertrophy to decompensated heart failure.
机译:心力衰竭是导致死亡的主要原因,正在达到流行病的程度。它是一种临床综合征,可归因于多种因素,首先是称为肥大的代偿性反应,然后是代偿性反应,最终导致衰竭。当心脏长时间处于病理性压力超负荷(PO)或体积超负荷(VO)时,会引发心力衰竭。迄今为止,还没有比较的连续超声心动图研究来概述PO与VO大鼠肥大的进展。我们假设PO或VO会引起差异性的心脏重塑,从而导致收缩功能障碍和随后的心力衰竭。为了解决这个假设,我们使用超声心动图研究了PO和VO引起的肥大大鼠模型中心脏结构和功能的系列进展。 PO或VO分别通过执行腹主动脉束带或主动脉腔分流术来诱导,而在两种模式下在关键时间间隔通过M型和多普勒超声心动图评估了心脏的结构和功能。 PO大鼠表现出进行性壁增厚与同心肥大相符,而VO大鼠表现出明显的左心室扩张与离心性肥厚相符。与PO相比,VO早期发生收缩功能障碍。 PO中舒张功能障碍很明显,而VO显示舒张功能增强的迹象。在代偿性肥大发展为代偿性心力衰竭期间,PO和VO引起心脏结构和功能的差异变化。

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