• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >Heart size-independent analysis of myocardial function in murine pressure overload hypertrophy.
【24h】

Heart size-independent analysis of myocardial function in murine pressure overload hypertrophy.

机译：小鼠压力超负荷肥大中心肌功能的独立于心脏大小的分析。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Pressure overload cardiac hypertrophy may be a compensatory mechanism to normalize systolic wall stress and preserve left ventricular (LV) function. To test this concept, we developed a novel in vivo method to measure myocardial stress (sigma)-strain (epsilon) relations in normal and hypertrophied mice. LV volume was measured using two pairs of miniature omnidirectional piezoelectric crystals implanted orthogonally in the endocardium and one crystal placed on the anterior free wall to measure instantaneous wall thickness. Highly linear sigma-epsilon relations were obtained in control (n = 7) and hypertrophied mice produced by 7 days of transverse aortic constriction (TAC; n = 13). Administration of dobutamine in control mice significantly increased the load-independent measure of LV contractility, systolic myocardial stiffness. In TAC mice, systolic myocardial stiffness was significantly greater than in control mice (3,156 +/- 1,433 vs. 1,435 +/- 467 g/cm(2), P < 0.01), indicating enhanced myocardial contractility with pressure overload. However, despite the increased systolic performance, both active (time constant of LV pressure decay) and passive (diastolic myocardial stiffness constant) diastolic properties were markedly abnormal in TAC mice compared with control mice. These data suggest that the development of cardiac hypertrophy is associated with a heightened contractile state, perhaps as an early compensatory response to pressure overload.
机译：压力超负荷心肌肥大可能是使收缩壁压力正常化并保持左心室（LV）功能的一种补偿机制。为了测试这个概念，我们开发了一种新颖的体内方法来测量正常和肥大小鼠的心肌压力（sigma）-应变（epsilon）关系。使用两对正交植入心内膜的微型全向压电晶体和一个置于前自由壁上的晶体测量瞬时壁厚，从而测量左室容积。在对照组（n = 7）和肥大小鼠中，通过主动脉缩窄7天（TAC; n = 13）获得了高度线性的sigma-ε关系。在对照组小鼠中给予多巴酚丁胺可显着增加左心室收缩力，收缩期心肌硬度的负荷独立测量。在TAC小鼠中，收缩期心肌硬度显着高于对照小鼠（3,156 +/- 1,433 vs. 1,435 +/- 467 g / cm（2），P <0.01），表明在压力超负荷时心肌收缩力增强。然而，尽管收缩性能增强，但与对照小鼠相比，TAC小鼠的主动（LV压力衰减的时间常数）和被动（舒张心肌刚度常数）舒张特性均明显异常。这些数据表明，心脏肥大的发展与收缩状态的升高有关，也许是对压力超负荷的早期代偿性反应。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号