油酸所致急性肺水肿机制的研究

MECHANISM STUDIES OF OLEIC ACID-INDUCED ACUTE LUNG EDEMA

为了探讨呼吸窘迫综合征（Respiratory Distress Syndrome简称RDS）时急性肺水肿的机制，我们应用静脉注射油酸引起RDS模型研究的肺血管及血管内皮细胞的损伤变化。我们的实验发现肺损伤后系数明显升高，证实油酸引起肺损伤早期确实存在急性肺水肿；肺微血管面积密度增大定量反映肺组织中血管扩张，充血；血浆6-酮-PGF1α和TxB2含量变化以及Ｐ／Ｔ比值呈增加趋势提示该变化与血扩张有密切关系；血清ACE活性升高表明血管内皮细胞膜受到损伤；此外形态学观察也发现血内皮细胞有形态及功能改变，提示血管内皮细胞是 引起急性肺水肿更直接的原因。

With oleic acid-induced RDS model in rats, the changes of pulmonary microvascu lature and endothelial cells were studied to learn more about the mechanism of acute lung edema. We found that lung coefficient was increased remarkedly and this proved the existence of edema; The rising of pulmonary microvascular density quantitively demonstrated the vascular dilatation and congestion.The changes of 6-Keto-PGF_1α and TxB_2contents in plasma and the rising tendency of P / T ratio showed their relation to the vascular dilatation. Higher level of ACE activity in serum after infusion, as well as morphologic and physiologic changes of endothelial cells induced the conclusion that endothelial injury might be a direct cause of acute lung edema.