Florenzano F, Glantz S A
Am J Physiol. 1987 May;252(5 Pt 2):H969-84. doi: 10.1152/ajpheart.1987.252.5.H969.
Increased end-diastolic wall stress has been hypothesized to stimulate left ventricular (LV) hypertrophy following volume overload. We instrumented intact-chest dogs with radiopaque markers in both ventricles and created volume overload by puncturing one aortic valve cusp. End-diastolic stress increased immediately, then fell over 3 mo as the heart hypertrophied. End-systolic stress did not change significantly. Chamber contractility, quantified as Emax, the end-systolic pressure-volume line slope, increased. Emax normalized by multiplying by LV mass increased following the lesion before but not after beta-blockade with propranolol and did not change significantly over time, suggesting that chamber contractility changed because of increased mass and sympathetic tone rather than changed intrinsic muscle function. LV mass did not initially correlate with lesion size, but steady-state mass did. Over the range of lesions we produced, increased end-diastolic wall stress appears to stimulate hypertrophy at a fixed rate, which stops when end-diastolic wall stress has been reduced to an acceptable level.
舒张末期壁应力增加被认为会在容量超负荷后刺激左心室（LV）肥厚。我们在完整胸腔的犬类双侧心室植入不透射线的标记物，并通过穿刺一个主动脉瓣尖来造成容量超负荷。舒张末期应力立即增加，然后在心脏肥厚的3个月内下降。收缩末期应力没有显著变化。以Emax（收缩末期压力-容积线斜率）量化的心室收缩性增加。在病变前，通过乘以左心室质量进行归一化的Emax增加，但在用普萘洛尔进行β受体阻滞剂治疗后没有增加，并且随时间没有显著变化，这表明心室收缩性的改变是由于质量增加和交感神经张力增加，而不是内在肌肉功能的改变。左心室质量最初与病变大小无关，但稳态质量相关。在我们产生的病变范围内，舒张末期壁应力增加似乎以固定速率刺激肥厚，当舒张末期壁应力降低到可接受水平时肥厚停止。
