β－受体激动剂对血小板激活因子致肺水肿的抑制作用

Inhibitory Effects of β-Adrenoceptor Agonist on Lung Edema Induced by Platelet-activating Factor

用离体灌注肺模型研究了异丙肾上腺素（ＩＰＮ）对血小板激活因子（ＰＡＦ）所致肺血管壁通透性增高的抑制作用。豚鼠肺用Ｔｒｉｓ－缓冲Ｒｉｎｇｅｒ液作恒流灌注，通过气管将肺悬吊于张力传感器上，连续记录肺重量变化。用恒压灌注测定微血管对液体的滤过系数（Ｋｆ）。结果，灌注液中加１０－９ｍｏｌ／ＬＰＡＦ，灌注１５ｍｉｎ后肺增重由对照组的０．３２±０．０８ｇ上升到２．４４±０．４４ｇ，Ｐ＜０．０１，Ｋｆ值由对照组的３．０６±１．０２×１０－３上升到１６．８４±１．５０±１０－３（ｍｌ·ｍｉｎ－１·ｋＰａ－１）。如在ＰＡＦ作用前先加β－受体激动剂ＩＰＮ１０－４ｍｏｌ／Ｌ可明显降低ＰＡＦ引起的肺增重和Ｋｆ变化；β－受体阻断剂心得安（２．５μｇ／ｍｌ）能逆转ＩＰＮ的作用。说明ＩＰＮ通过激活β－受体增强血管壁屏障功能，减轻ＰＡＦ引起的水肿。

This study evaluated the inhibitory effects of isoproterenol(IPN) on lung vascular permeability increase induced by platelet-activating factor(PAF) in isolated guinea-pig lungs. The lungs were volumestatically perfused with Tris-buffered Ringer's solution, and were suspended from a force transducer through the trachea. Lung weight was continuously recorded. Fluid filtration coeffi cient (Kf) of microvascular bed was determined under pressure static perfosion. The results showed that 15 min after addition of PAF 10-9mol/L to the perfusate, the lung weight gain increased from control value of 0.32±0.08 g to 2.44±0.44g and Kf increased from 3.06±1 .02 ×10-3 to 16.84±1.50 ×10-3 (ml· min-1·kpa-1). Preaddition of β-agonist isoproterenol (IPN) 10-4mol/L significantly reduced the changes in lung weight gain and Kf induced by PAF. The effects of IPN were reversed by β-antagonist propranolol (PPN) (2. 5μg/ml), indicating that IPN enhanced vascular barrier function and reduced PAF-induced lung edema via activation of β-adrenoceptors.