Ohkuda K, Nakahara K, Binder A, Staub N C
J Appl Physiol Respir Environ Exerc Physiol. 1981 Oct;51(4):887-94. doi: 10.1152/jappl.1981.51.4.887.
We studied the effects of continuous intravenous air embolization on lung fluid balance in unanesthetized sheep. Following a 2-h base line, we infused 300-micrometers-diam air bubbles into the pulmonary artery at a rate sufficient to increase pulmonary vascular resistance by 60-300% and for periods of 0.25-3 h. Air emboli produced a dose- and duration-dependent increase in lung lymph and protein flow due mainly to an increase in endothelial barrier permeability but also to elevated pressure in the over-perfused microcirculation. When we stopped the air infusion, the vascular resistance fell as the air emboli were reabsorbed. Lung lymph and protein flow increased further and then returned slowly to base line with a half-time proportional to the duration of embolization. Increasing left atrial pressure during air embolization caused an increase in lymph flow and protein clearance and an average decrease of 15 Torr in arterial O2 tension, all changes in excess of that caused by either increased pressure or air emboli alone.
我们研究了持续静脉空气栓塞对未麻醉绵羊肺液体平衡的影响。在2小时的基线期后,我们以足以使肺血管阻力增加60%-300%的速率,向肺动脉内注入直径为300微米的气泡,持续时间为0.25-3小时。空气栓塞导致肺淋巴液和蛋白质流量呈剂量和时间依赖性增加,这主要是由于内皮屏障通透性增加,也与过度灌注的微循环中压力升高有关。当我们停止注入空气时,随着空气栓子被吸收,血管阻力下降。肺淋巴液和蛋白质流量进一步增加,然后缓慢恢复到基线水平,其半衰期与栓塞持续时间成正比。在空气栓塞期间增加左心房压力会导致淋巴液流量和蛋白质清除率增加,动脉血氧张力平均降低15托,所有这些变化都超过了单独由压力增加或空气栓塞所引起的变化。