Hyperfunction with normal inotropic state of the hypertrophied left ventricle.
Hyperfunction with normal inotropic state of the hypertrophied left ventricle.
复制标题
肥大的左心室功能亢进且正性肌力状态正常。
作者：
S. Sasayama;D. Franklin;J. Ross
清醒的狗在升主动脉周围装有可充气袖带，在左心室（LV）装有高保真微压计，并使用超声晶体对测量LV壁厚度和LV内径。计算室壁应力（WSt）和室壁平均缩短速度（VCF）。然后在急性主动脉缩窄过程中，在持续性主动脉缩窄诱导慢性肥厚之前和之后，在一系列匹配的收缩压范围内分析单次收缩中的平均力-速度关系和WSt-直径环。在正常的左室收缩压和每一个匹配的左室收缩压水平，室壁缩短速度增加肥厚的心室。然而，力-速度的关系，通过相关的平均VCF平均WSt在不同的应力水平下降在控制过程中相同的关系。左室内径与射血末压力的线性关系在肥厚的心室中左移，表明左室缩短增强。然而，在射血末期的线性WST-直径关系在对照组和肥厚心脏中没有差异。这些结果表明，心室肥厚的压力超负荷表现为泵功能亢进，但其心肌有正常水平的正性肌力状态。
Conscious dogs were instrumented with an inflatable cuff around the ascending aorta, a high-fidelity micromanometer in the left ventricle (LV), and pairs of ultrasonic crystals for measurements of LV wall thickness and internal LV diameter. Wall stress (WSt) and mean velocity of wall shortening (VCF) were calculated. Mean force-velocity relations and WSt-diameter loops in single contractions were then analyzed over a range of matched systolic pressures during acute aortic constrictions both before and after induction of chronic hypertrophy by sustained aortic constriction. At normal LV systolic pressures and at each matched level of systolic LV pressure, wall shortening velocity was increased in the hypertrophied ventricle. However, force-velocity relations obtained by relating mean VCF to mean WSt at various stress levels fell on the same relation as during control. The linear relation between LV diameter and pressure at the end of ventricular ejection was shifted to the left in the hypertrophied ventricle, indicating enhanced shortening. However, linear WSt-diameter relations at end-ejection were not different in control and hypertrophied hearts. These findings indicate that the ventricle hypertrophied by pressure overload exhibited hyperfunction as a pump but that its myocardium had a normal level of inotropic state.