Zimpfer M, Vatner S F
J Clin Invest. 1981 Feb;67(2):430-8. doi: 10.1172/JCI110051.
The effects of acute volume loading were examined on indices of left ventricular (LV) function in conscious, unrestrained and intact, tranquilized baboons. Experiments were conducted 1-3 mo after implantation of ultrasonic transducers to measure LV internal diameter and wall thickness, and miniature LV pressure gauges and aortic and left atrial catheters. In 10 intact, tranquilized baboons, rapid volume loading with saline increased LV end-diastolic pressure by 23.7+/-2.6 mm Hg, LV end-diastolic diameter by 7.8+/-1.5%, LV stroke work by 37.5+/-7.8%, while mean arterial pressure and peak LV wall stress did not change significantly. Despite the increase in preload and activation of the Frank-Starling mechanism, LV dP/dt(max) and the maximum velocity of myocardial fiber shortening (LV dD/dt(max)) did not change. Volume loading after beta-adrenergic or combined beta-adrenergic and cholinergic blockades or volume loading with blood instead of saline also failed to augment LV dP/dt(max) and LV dD/dt(max) despite the increase in preload. In order to volume load the baboons in the conscious state, a radiofrequency (RF) interrogator system was devised, which upon receipt of a radio command, activated a battery operated pump to infuse 1,000 ml of saline i.v. to the baboons. In these experiments, preload rose, i.e., LV end-diastolic diameter increased by 13.9+/-2.1% and the Frank-Starling mechanism could be demonstrated, i.e., stroke work rose by 42.8+/-7.4%, but LV dP/dt(max) and LV dD/dt(max) did not change. After preload was depressed by hemorrhage, the rapid infusion of either blood or saline increased LV dP/dt(max) by 92.7+/-18.5% and LV dD/dt(max) by 64.3+/-10.1%. Thus, acute volume loading in the conscious baboons increased LV end-diastolic size and even stroke work substantially. However, preload dependency of LV dP/dt(max) and the maximum velocity of myocardial fiber shortening was only encountered at low levels of LV preload.
在清醒、未受束缚且完整、安静的狒狒身上,研究了急性容量负荷对左心室(LV)功能指标的影响。在植入超声换能器以测量左心室内径和壁厚、微型左心室压力计以及主动脉和左心房导管1 - 3个月后进行实验。在10只完整、安静的狒狒中,用生理盐水快速容量负荷使左心室舒张末期压力升高23.7±2.6 mmHg,左心室舒张末期直径增加7.8±1.5%,左心室每搏功增加37.5±7.8%,而平均动脉压和左心室壁峰值应力无显著变化。尽管前负荷增加且Frank - Starling机制激活,但左心室dp/dt(max)和心肌纤维缩短最大速度(左心室dD/dt(max))未改变。在β - 肾上腺素能或β - 肾上腺素能与胆碱能联合阻断后进行容量负荷,或用血液而非生理盐水进行容量负荷,尽管前负荷增加,也未能增加左心室dp/dt(max)和左心室dD/dt(max)。为了在清醒状态下对狒狒进行容量负荷,设计了一种射频(RF)询问器系统,该系统在接收到无线电指令后,启动一个电池驱动的泵,静脉内给狒狒输注1000 ml生理盐水。在这些实验中,前负荷升高,即左心室舒张末期直径增加13.9±2.1%,并且可以证明Frank - Starling机制,即每搏功升高42.8±7.4%,但左心室dp/dt(max)和左心室dD/dt(max)未改变。在出血使前负荷降低后,快速输注血液或生理盐水使左心室dp/dt(max)增加92.7±18.5%,左心室dD/dt(max)增加64.3±10.1%。因此,清醒狒狒的急性容量负荷显著增加了左心室舒张末期大小甚至每搏功。然而,左心室dp/dt(max)和心肌纤维缩短最大速度对前负荷的依赖性仅在左心室前负荷较低水平时出现。