Bressack M A, Morton N S, Hortop J
McGill University, Montreal Children's Hospital Research Institute, Quebec, Canada.
Circ Res. 1987 Nov;61(5):659-69. doi: 10.1161/01.res.61.5.659.
We investigated the physiologic effects of normal saline versus 5% albuminated saline fluid resuscitation on 10-12-day-old piglets infected with group B streptococci for four hours. After intravenously receiving 1 X 10(10) bacteria/kg over 45 minutes, one group was untreated while the two fluid-treated groups received enough intravenous fluid to maintain the baseline cardiac output. An increase in the resistance to venous blood return was the major limitation to cardiac output. The resistance nearly quadrupled in the untreated piglets as shown by a 50% decrease in cardiac output with a nearly doubling of the driving pressure for venous return (mean circulatory pressure was normal and atrial pressures decreased by 70%). In both fluid-treated groups, resistance doubled as shown by an unchanged cardiac output with a doubling of the driving pressure (mean circulatory pressure increased by 50%) and atrial pressures remained at baseline). Blood volume was 9% below control in the untreated group and 13% above control in both fluid-treated groups. Much more crystalloid (155 ml/kg) than colloid (58 ml/kg) was necessary to maintain baseline cardiac output; this resulted in a 36% decrease in the plasma protein oncotic pressure of the former group and a 15% increase in the oncotic pressure of the latter group. Organ edema formation (ileum, pancreas, kidney, adrenal gland, lung) occurred only in the saline-treated animals. We conclude that increased resistance to venous return was the primary cause of shock in our model and that this can be effectively treated by giving enough intravenous fluid to elevate the mean circulatory pressure. However, if the plasma protein oncotic pressure is also lowered (saline group), organ edema results.
我们研究了生理盐水与5%白蛋白盐水液体复苏对感染B组链球菌4小时的10 - 12日龄仔猪的生理影响。在45分钟内静脉注射1×10(10) 个细菌/kg后，一组不进行治疗，而两个液体治疗组接受足够的静脉液体以维持基线心输出量。静脉血回流阻力增加是心输出量的主要限制因素。未治疗的仔猪阻力几乎增加了四倍，表现为心输出量下降50%，静脉回流驱动压力几乎翻倍（平均循环压力正常，心房压力下降70%）。在两个液体治疗组中，阻力翻倍，表现为心输出量不变，驱动压力翻倍（平均循环压力增加50%），心房压力保持在基线水平。未治疗组的血容量比对照组低9%，两个液体治疗组的血容量比对照组高13%。维持基线心输出量需要更多的晶体液（155 ml/kg）而非胶体液（58 ml/kg）；这导致前一组血浆蛋白胶体渗透压下降36%，后一组胶体渗透压增加15%。器官水肿形成（回肠、胰腺、肾脏、肾上腺、肺）仅发生在生理盐水治疗的动物中。我们得出结论，静脉回流阻力增加是我们模型中休克的主要原因，通过给予足够的静脉液体以提高平均循环压力可有效治疗休克。然而，如果血浆蛋白胶体渗透压也降低（生理盐水组），则会导致器官水肿。
