D'Orio V, Wahlen C, Naldi M, Fossion A, Juchmes J, Marcelle R
Medical Intensive Care Unit, State University of Liège, Belgium.
Crit Care Med. 1989 Dec;17(12):1314-9. doi: 10.1097/00003246-198912000-00014.
The aim of the present study was to determine possible effects of Escherichia coli endotoxin on peripheral vascular compliance and relate them to concomitant central hemodynamic disturbances. Endotoxin was infused at 0.25 micrograms/kg.min during 2 h in six anesthetized dogs, while six additional animals served as controls. Vascular compliance of the systemic circulation was calculated in intact animals from the changes in CVP after known changes in systemic blood volume. In control dogs, vascular compliance averaged 2.3 ml/mm Hg.kg body weight. During slow endotoxin infusion, cardiovascular effects were measurable only after a certain period of time had elapsed from the start of endotoxin insult and consisted of hypotension associated with systemic vasodilation. Systemic BP decreased gradually from 124 to 68 mm Hg while vascular compliance was finally increased by 100%, when compared to control values. This latter rise was responsible for a reduction in the cardiac preloads. Pulmonary wedge pressure and CVP were decreased from 7.1 to 3.4 and from 4.5 to 2.6 mm Hg, respectively. However, parallel to the decrease in left ventricular preload, endotoxin induced a progressive decrease in left ventricular afterload. Because of the balance in ventricular loading, cardiac output remained almost unchanged. After volume loading (dextran 30 ml/kg), cardiac output was remarkably increased from 3.28 to 6.24 L/min.m2 while peripheral vasodilation was not affected by this maneuver. It is concluded that low dose endotoxin infusion induces in dogs a hemodynamic pattern similar to human sepsis. The left ventricular loading changes are related to an enhanced systemic vascular compliance from 2.3 to 4.5 ml/mm Hg.kg. High flow shock state is encountered provided peripheral blood pooling is compensated by adequate volume replacement.
本研究的目的是确定大肠杆菌内毒素对外周血管顺应性的可能影响,并将其与伴随的中心血流动力学紊乱联系起来。在6只麻醉犬中,以0.25微克/千克·分钟的速度输注内毒素,持续2小时,另外6只动物作为对照。在完整动物中,根据已知的全身血容量变化后中心静脉压(CVP)的变化计算体循环的血管顺应性。在对照犬中,血管顺应性平均为2.3毫升/毫米汞柱·千克体重。在内毒素缓慢输注期间,只有在内毒素损伤开始后的一段时间后才能检测到心血管效应,包括与全身血管扩张相关的低血压。全身血压从124毫米汞柱逐渐降至68毫米汞柱,而与对照值相比,血管顺应性最终增加了100%。后者的升高导致心脏前负荷降低。肺楔压和中心静脉压分别从7.1毫米汞柱降至3.4毫米汞柱和从4.5毫米汞柱降至2.6毫米汞柱。然而,与左心室前负荷降低同时,内毒素导致左心室后负荷逐渐降低。由于心室负荷的平衡,心输出量几乎保持不变。在容量负荷(右旋糖酐30毫升/千克)后,心输出量从3.28升/分钟·平方米显著增加至6.24升/分钟·平方米,而外周血管扩张不受此操作影响。结论是,低剂量内毒素输注在犬中诱导出与人类败血症相似的血流动力学模式。左心室负荷变化与全身血管顺应性从2.3毫升/毫米汞柱·千克增加至4.5毫升/毫米汞柱·千克有关。如果通过适当的容量替代来补偿外周血液淤积,就会出现高流量休克状态。