Effects of remifentanil on lipopolysaccharide-induced acute lung injury in rabbits

Abstract

Objective To investigate the effects of remifentanil on lipopolysaccharide ( LPS)-induced acute lung injury (ALI) in rabbits.Methods Thirty healthy male New Zealand white rabbits weighing 2.5-3.5 kg were randomly divided into 5 groups ( n = 6 each) : group Ⅰ control (group C) ;group Ⅱ ALI;group Ⅲ, Ⅳ, Ⅴ low, median and high dose RF + LPS (group LR, MR, HR) . The animals were anesthetized with intravenous 3% pentobarbital sodium 30 mg/kg, tracheostomized and mechanically ventilated. The carotid artery and jugular vein were cannulated for MAP and HR monitoring, blood sampling, and fluid and drug administration. LPS 0.5 mg/kg in 10 ml of normal saline (NS) was infused over 30 min in group Ⅱ-Ⅴ. Remifentanil 0.2, 0.4 or 0.8 μg·kg~(-1)·min~(-1) was infused starting from 15 min before LPS administration until the death of the animals. MAP, HR, peak airway pressure (P_(peak) ), PaO_2 and plasma intercellular adhesion molecule 1 (ICAM-1) concentration were measured immediately before LPS infusion (T_0, baseline) and at 1, 2.5 and 5.5 h after the end of LPS infusion. The animals were killed and the lungs were immediately removed for microscopic examination and determination of W/D lung weight ratio. Results MAP, HR and PaO_2 were significantly decreased while W/D ratio and P_(peak) were significantly increased after iv LPS infusion as compared with control group. LPS significantly increased plasma ICAM-1 concentration and damaged the structure of lung tissue. Remifentanil infusion significantly attenuated the LPS-induced changes in a dose-dependent manner. Conclusion RF has protective effect against LPS-induced ALI and inhibition of ICAM-1 expression is involved in the mechanism. Key words: Piperidines; Endotoxemia; Respiratory distress syndrome; adult