Mayer J E, Kersten T E, Humphrey E W
J Thorac Cardiovasc Surg. 1981 Sep;82(3):358-64.
The effects of transfusion of whole blood clot emboli and aged citrated platelet-poor plasma on pulmonary capillary permeability were investigated in anesthetized sheep by continuous collection of pulmonary lymph. Changes in lymph flow and lymph-to-plasma ratios (CL/CP) for albumin and globulin were utilized to detect changes in permeability. Infusion of 0.5 cc/kg of finely (less than or equal to 1 mm) diced autologous whole blood clot resulted in a 170% increase in lymph flow over control with no change in CL/CP for albumin or globulin. Infusion of 1 cc/kg of autologous clot increased lymph flow 180% over control and increased CL/CP for albumin and globulin. Infusion of homologous platelet-poor plasma caused greater increases in lymph flow without changes in CL/CP. Changes in each of these three groups were consistent with increased permeability. Balloon occlusion of one main pulmonary artery was induced without a fall in cardiac output and resulted in no change in lymph flow of CL/CP despite a rise in pulmonary vascular resistance (PVR). Femoral arteriovenous fistulas were created to increase cardiac output, but no change in lymph flow or CL/CP occurred. The results in these latter two experiments suggest that increased perfusion per unit lung capillary bed or increased PVR were not primarily responsible for the changes observed in the emboli-treated and plasma-infused animals. Since both emboli and aged platelet-poor plasma increased pulmonary capillary permeability, the permeability increasing factor appears to be humoral in origin. Similar humoral factors may be important in the pathogenesis of the adult respiratory distress syndrome in man.
通过持续收集肺淋巴液,在麻醉的绵羊中研究了全血凝块栓子和陈旧枸橼酸盐贫血小板血浆输注对肺毛细血管通透性的影响。利用淋巴液流量以及白蛋白和球蛋白的淋巴 - 血浆比率(CL/CP)变化来检测通透性变化。输注0.5 cc/kg精细(小于或等于1毫米)切碎的自体全血凝块导致淋巴液流量比对照组增加170%,白蛋白或球蛋白的CL/CP无变化。输注1 cc/kg自体凝块使淋巴液流量比对照组增加180%,并使白蛋白和球蛋白的CL/CP增加。输注同种贫血小板血浆导致淋巴液流量增加幅度更大,而CL/CP无变化。这三组中的每一组变化均与通透性增加一致。在不降低心输出量的情况下诱导一条主肺动脉气囊阻塞,尽管肺血管阻力(PVR)升高,但淋巴液流量或CL/CP无变化。建立股动静脉瘘以增加心输出量,但淋巴液流量或CL/CP无变化。后两个实验的结果表明,单位肺毛细血管床灌注增加或PVR增加并非栓塞处理和血浆输注动物中观察到的变化的主要原因。由于栓子和陈旧贫血小板血浆均增加了肺毛细血管通透性,通透性增加因子似乎起源于体液。类似的体液因子可能在人类成人呼吸窘迫综合征的发病机制中起重要作用。