Rojas J, Green R S, Hellerqvist C G, Olegard R, Brigham K L, Stahlman M T
Pediatr Res. 1981 Jun;15(6):899-904. doi: 10.1203/00006450-198106000-00003.
To study the effects of Group B beta-hemolytic Streptococcus on the pulmonary circulation and lung fluid balance, live and heat-killed bacteria and their toxin were infused into an awake sheep lung-lymph preparation. In every case, the response was biphasic; there was an initial period of marked pulmonary hypertension and high flow of protein-poor lymph associated with tachypnea, chills, and fever. A second phase followed during which pulmonary vascular pressures returned to near baseline and remained stable, but lymph flow remained high. The changes seen in the initial phase resemble the previously reported response to mechanically increased pulmonary vascular pressure and suggest that the increase in fluid filtration is secondary to increased microvascular pressure. During the second phase after toxin infusion, the increase in lung lymph flow was paralleled by an increase in lymph protein clearance. This cannot be accounted for by the hemodynamic changes alone an suggests that the permeability of lung microvascular walls to protein was increased. It is concluded that group B beta-hemolytic streptococcal toxin in the sheep model causes pulmonary hypertension and increased pulmonary vascular permeability.
为研究B族β溶血性链球菌对肺循环和肺液体平衡的影响,将活的和热灭活的细菌及其毒素注入清醒绵羊的肺-淋巴制备模型中。在每种情况下,反应都是双相的;最初有一段明显的肺动脉高压期,伴有呼吸急促、寒战和发热,同时有蛋白质含量低的淋巴液高流量。随后进入第二阶段,在此期间肺血管压力恢复到接近基线水平并保持稳定,但淋巴液流量仍然很高。在初始阶段观察到的变化类似于先前报道的对机械性增加肺血管压力的反应,表明液体滤过增加是微血管压力增加的继发结果。在毒素注入后的第二阶段,肺淋巴液流量的增加与淋巴蛋白清除率的增加平行。这不能仅由血流动力学变化来解释,提示肺微血管壁对蛋白质的通透性增加。得出的结论是,绵羊模型中的B族β溶血性链球菌毒素会导致肺动脉高压和肺血管通透性增加。