Crozatier B, Caillet D, Thuillez C, Chevrier J L, Peronneau P, Hatt P Y
Am J Physiol. 1981 Mar;240(3):H354-60. doi: 10.1152/ajpheart.1981.240.3.H354.
The behavior of the end-systolic ventricular diameter was examined during control state, atrial pacing, and acute volume loading (VL) followed by methoxamine infusion in conscious dogs instrumented with a left ventricular micromanometer and ultrasonic crystals measuring internal diameter and wall thickness. Heart rate and systolic pressure were markedly increased by maximal VL but for moderate VL were minimally modified. Moderate VL increased end-diastolic diameter by 5% and end-systolic diameter by 2.9% with a significant increase of systolic stress. There was no common final pathway of shortening in the force-velocity-length diagram for different preloads. During methoxamine infusion, the end-systolic pressure-diameter points described a linear regression but points obtained during atrial pacing before VL were significantly shorter. We conclude that VL increases the total loading of the heart producing a lengthening of the end-systolic diameter when end-diastolic diameter is increased. This reduces the expression of the Starling mechanism and suggests caution when interpreting end-systolic pressure-diameter relations and derived indices for significantly different end-diastolic diameters.
在清醒犬身上,使用左心室微测压计以及测量内径和壁厚的超声晶体,研究了在对照状态、心房起搏、急性容量负荷(VL)及随后静脉输注甲氧明过程中,收缩末期心室直径的变化情况。最大容量负荷使心率和收缩压显著升高,但中度容量负荷时其变化极小。中度容量负荷使舒张末期直径增加5%,收缩末期直径增加2.9%,同时收缩期应力显著增加。在不同前负荷下的力-速度-长度关系图中,不存在共同的缩短终末途径。静脉输注甲氧明期间,收缩末期压力-直径点呈现线性回归,但容量负荷前心房起搏期间获得的点明显更短。我们得出结论,当舒张末期直径增加时,容量负荷增加了心脏的总负荷,导致收缩末期直径延长。这降低了Starling机制的表现,并提示在解释收缩末期压力-直径关系以及针对显著不同舒张末期直径得出的指标时应谨慎。