Contribution of ventricular remodeling to pathogenesis of heart failure in rats
Contribution of ventricular remodeling to pathogenesis of heart failure in rats
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DOI：
10.1152/ajpheart.2001.280.2.h674
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发表时间：
2001-02-01
影响因子：
4.8
通讯作者：
Janicki, JS
中科院分区：
文献类型：
--
作者：
Brower, GL;Janicki, JS
我们之前报道了大约50%的大鼠在肾下主动脉-腔静脉瘘后8周出现充血性心力衰竭（CHF）症状。然而，目前尚不清楚代偿性心室重构是否会持续超过8周，以及剩余的动物是否会发展为CHF或死亡。因此，本研究的目的是通过确定8周后左室（LV）重构和功能的发病率和死亡率以及时间反应来完成这种持续容量过载模型的表征。研究结果表明，左室肥大的上限、左室体积和顺应性的显著增加、基质金属蛋白酶活性和胶原体积分数与CHF的发展有关。慢性容量负荷21周后，有80%的发病率和死亡率。这些发现表明，CHF的发展是由显著的心室扩张触发的，一旦心肌肥厚反应耗尽，顺应性就会增加。
We previously reported an approximately 50% incidence of rats with symptoms of congestive heart failure (CHF) at 8 wk postinfrarenal aorto-caval fistula. However, it was not clear whether compensatory ventricular remodeling could continue beyond 8 wk or whether the remaining animals would have developed CHF or died. Therefore, the intent of this study was to complete the characterization of this model of sustained volume overload by determining the morbidity and mortality and the temporal response of left ventricular (LV) remodeling and function beyond 8 wk. The findings demonstrate an upper limit to LV hypertrophy and substantial increases in LV volume and compliance, matrix metalloproteinase activity, and collagen volume fraction associated with the development of CHF. There was an 80% incidence of morbidity and mortality following 21 wk of chronic volume overload. These findings indicate that the development of CHF is triggered by marked ventricular dilatation and increased compliance occurring once the myocardial hypertrophic response is exhausted.