Motohiro A, Furukawa T, Yasumoto K, Inokuchi K
Eur Surg Res. 1986;18(1):50-7. doi: 10.1159/000128505.
We investigated mechanisms related to the development of acute lung edema, as induced by oleic acid in adult mongrel dogs. The intravenous injection of oleic acid (0.04 ml/kg) was considered to induce a permeability edema, as an enhancement of transvascular protein clearance was observed after the injection. The effects of oleic acid injection on systemic blood pressure (SBP), pulmonary arterial pressure (PAP), pulmonary arterial wedge pressure (PAWP), cardiac output (CO) and airway pressure (AWP) were measured. A significant decrease in CO and increase in AWP were evident after the injection, but there were no changes in SBP, PAP and PAWP. Treatment of the animals with prostaglandin I2 (PGI2) did not alter the induction of edema by oleic acid. However, the decrease in CO and increase in AWP were normalized by treatment with PGI2. Blood platelet count was not affected by oleic acid given in a dose of 0.04 ml/kg. To determine the direct effect of oleic acid on the vascular endothelium, the agent was injected through a catheter placed in the pulmonary artery. Electron microscopic examination revealed severe vacuolation on the endothelium of the pulmonary artery after only 1 min of exposure to oleic acid. Increased permeation of Evans blue into the subendothelial tissue was also observed with oleic acid treatment, compared with findings in the controls. These results indicate that the lung edema induced by oleic acid is due to an increased protein clearance, probably through a direct toxic effect on the vascular endothelium rather than an indirect toxic effect of chemical mediators released from the aggregated platelets.
我们研究了成年杂种犬油酸诱导的急性肺水肿发生发展的相关机制。静脉注射油酸(0.04 ml/kg)被认为可诱导通透性水肿,因为注射后观察到跨血管蛋白清除增强。测量了油酸注射对体循环血压(SBP)、肺动脉压(PAP)、肺动脉楔压(PAWP)、心输出量(CO)和气道压(AWP)的影响。注射后CO显著降低,AWP升高,但SBP、PAP和PAWP无变化。用前列腺素I2(PGI2)治疗动物并没有改变油酸诱导的水肿。然而,用PGI2治疗可使CO降低和AWP升高恢复正常。给予0.04 ml/kg剂量的油酸对血小板计数无影响。为了确定油酸对血管内皮的直接作用,将该药物通过置于肺动脉的导管注入。电子显微镜检查显示,仅在暴露于油酸1分钟后,肺动脉内皮就出现严重空泡化。与对照组相比,油酸处理后还观察到伊文思蓝向血管内皮下层组织的渗透增加。这些结果表明,油酸诱导的肺水肿是由于蛋白清除增加,可能是通过对血管内皮的直接毒性作用,而不是聚集血小板释放的化学介质的间接毒性作用。