Candidate mechanical stimuli for hypertrophy during volume overload
Candidate mechanical stimuli for hypertrophy during volume overload
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DOI：
10.1152/japplphysiol.00834.2003
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发表时间：
2004-10-01
影响因子：
3.3
通讯作者：
Holmes, JW
中科院分区：
文献类型：
--
作者：
Holmes, JW
感知和响应机械输入的肌细胞系统可能被肌细胞所经历的随时间变化的长度或力信号的任何数量的特征激活。因此，我们的特点是左心室容量和室壁应力信号在早期容量超负荷与高空间和时间分辨率。在手术建立肾下动静脉瘘或假手术后4天和7天，在开胸异氟烷麻醉的雄性Sprague-Dawley大鼠中测量左心室压力和容积。采用一个简单的厚壁椭球体模型计算了壁面平均应力。与之前的报告一致，该手术模型在第7天产生了66%的心输出量增加和10%的左心室质量增加。一些功能的时变容量信号（最大值，平均值，振幅，上升和下降率）显着改变早期容量超负荷，而许多其他建议的肥大刺激，包括峰值收缩期壁应力和舒张期应变，没有。将血流动力学变量更普遍地视为时变信号，使我们能够识别更广泛的肥大候选机械刺激（包括文献中先前未提出的一些），而不是专注于心动周期中的标准时间点。我们得出结论，功能随时间变化的心室容积信号和相关的局部变形可能会驱动肥大在容量超负荷，并提出这些功能的体积信号，也改变压力超负荷可能是最有趣的候选人进行进一步探索。
A myocyte system that senses and responds to mechanical inputs might be activated by any number of features of the time-varying length or force signals experienced by the myocytes. We therefore characterized left ventricular volume and wall stress signals during early volume overload with high spatial and temporal resolution. Left ventricular pressure and volume were measured in open-chest isoflurane-anesthetized male Sprague-Dawley rats 4 and 7 days after surgical creation of an infrarenal arteriovenous fistula or sham operation. Mean wall stresses were calculated by using a simple thick-walled ellipsoidal model. Consistent with previous reports, this surgical model produced a 66% increase in cardiac output and a 10% increase in left ventricular mass by day 7. A number of features of the time-varying volume signal (maximum, mean, amplitude, rates of rise and fall) were significantly altered during early volume overload, whereas many other proposed hypertrophic stimuli, including peak systolic wall stress and diastolic strain, were not. Treating hemodynamic variables more generally as time-varying signals allowed us to identify a wider range of candidate mechanical stimuli for hypertrophy (including some not previously proposed in the literature) than focusing on standard time points in the cardiac cycle. We conclude that features of the time-varying ventricular volume signal and related local deformations may drive hypertrophy during volume overload and propose that those features of the volume signal that also change during pressure overload might be the most interesting candidates for further exploration.