Ren X D, Huang S J, Sun J J, Zhu Z G
Department of Pharmacology, Sun Yat-Sen University of Medical Sciences, Guangzhou, P.R. China.
Int J Immunopharmacol. 1994 Nov;16(11):969-75. doi: 10.1016/0192-0561(94)90050-7.
The protective effect of cobra venom factor (CVF), separated from the venom of Naja naja atra, on pulmonary injury induced by oleic acid was reported. The blood gas tensions, tidal volume, transthoracic pressure and pulmonary arterial pressure in anaesthetized dogs were continually monitored. The experimental results showed that CVF, given 20 h before the dosage depleting complements exceed 95%, significantly attenuated oleic acid-induced pulmonary dysfunction, including hypoxemia, increasing veno-arterial shunt and P(A-a)O2 and decreasing dynamic compliance and pulmonary blood flow. Histological examination of lung tissues after the experiment also showed improvement of hyaline membrane formation, alveolar haemorrhage and pulmonary arteriolar thrombosis. It was evident that the depletion of serum complements by CVF inhibited the development of lung injury induced by oleic acid. CVF might be a potentially useful drug for the treatment of respiratory distress syndrome in the near future.
报道了从眼镜蛇毒中分离出的眼镜蛇毒因子(CVF)对油酸诱导的肺损伤的保护作用。持续监测麻醉犬的血气张力、潮气量、跨胸压和肺动脉压。实验结果表明,在补体耗竭超过95%的剂量前20小时给予CVF,可显著减轻油酸诱导的肺功能障碍,包括低氧血症、静脉-动脉分流增加、P(A-a)O2升高以及动态顺应性和肺血流量降低。实验后肺组织的组织学检查也显示透明膜形成、肺泡出血和肺小动脉血栓形成有所改善。显然,CVF导致的血清补体耗竭抑制了油酸诱导的肺损伤的发展。CVF可能在不久的将来成为治疗呼吸窘迫综合征的一种潜在有用药物。