摘要
目的 研究静脉注射前列腺素E1(PGE1)能否阻止酸吸入性急性呼吸窘迫综合征(ARDS)的发生。方法 2 0只新西兰兔在稀HCl经右支气管滴入后随机分成两组 :(1)损伤组 (n =10 )在酸滴入后维持机械通气 ,未行其它治疗 ;(2 )治疗组 (n =10 )在酸滴入后即刻缓慢静注PGE1并维持。在基础状态及酸滴入后记录血气、气道压力并抽动脉血测定 6 K PGF1α、TXB2 、NO-2 /NO-3 和ET 1,动物处死后测定右肺的湿干比 (W /D)值及测定右肺支气管肺泡灌洗液 (BALF)中总蛋白 (TP)的水平 ,并作肺组织形态学观察。结果 治疗组在酸滴入后血氧分压 (PaO2 )显著高于损伤组。治疗组血浆 6 K PGF1α和NO-2 /NO-3 水平显著高于损伤组 ,而血浆TXB2 和ET 1水平显著低于损伤组 ,治疗组右肺W/D和TP显著低于损伤组。损伤组右肺呈弥漫性炎性损伤 ,而治疗组则见损伤呈局灶性 ,且其病理损伤程度较损伤组明显减轻。结论 (1)酸吸入后即刻应用PGE1可减轻ARDS的范围和严重程度 ;(2 )PGE1保护了肺血管内皮细胞 ,使内源性PGI2 /TXA2 和NO /ET 1的产生保持平衡 ,有利于减轻ARDS。
Objective The purpose of this study was to evaluate the effect of prostaglandin E 1 (PGE 1) on blocking the development of acute respiratory distress syndrome (ARDS) induced by acid aspiration. Methods Twenty new Zealand rabbits were used. Dilute HCl was instilled into right bronchus of the rabbits. The rabbits were then divided randomly into two groups: injury group and treatment group. In injury group (n=10) rabbits received no treatment except mechanical ventilation. In treatment group (n=10) immediately after acid instillation the rabbits received an intravenous bolus of PGE 1 followed by a continuous infusion. Blood gas, airway pressure and dynamic and static compliance were measured before and after acid instillation. Blood samples were taken from artery for determination of 6-k-PGF 1α, TXB 2,NO 2 -/NO 3 - and ET-1. The animals were killed and the wet/dry lung weight (W/D) ratio and total protein of bronchoalveolar lavage fluid(BALF) of right lung were measured. Microscopic examination of the lung was done. Results In treatment group PaO 2 was significantly higher than that in injury group after acid instillation. Plasma 6-k-PGF 1α and NO - 2/NO - 3 levels were significantly higher in treatment group while plasma TXB 2 and ET-1 levels were significantly lower. W/D ratio and TP of BALF of right lung were significantly lower in treatment group. The inflammatory changes were diffuse in injury group while in treatment group they were localized and less severe. Conclusions PGE1 can lessen severity of ARDS induced by acid aspiration. It may protect pulmonary vascular endothelial cells through maintaining the balance between PGI 2 and TXA 2 and that between NO and ET-1 .
出处
《中华麻醉学杂志》
CAS
CSCD
北大核心
2001年第1期28-31,共4页
Chinese Journal of Anesthesiology
基金
上海市医学领先专业科研基金资助项目 (批准号 9930 2 7)
