粘附分子和白介素8在早期急性呼吸窘迫综合征中的作用研究

目的 :探讨急性失血致低血容量性休克后低剂量内毒素动物模型中血浆白介素 8(IL 8)、细胞间粘附分子 1(ICAM 1)、血管内皮粘附分子 1(VCAM 1)水平的改变及其与血浆 IL 1β水平的关系。方法 :2 2只新西兰白兔随机分成 4组 :1低血容量性休克组 (休克组 ,6只 ) :急性失血持续 1小时 ,以心排血量低于基础值 40 %为准 ,休克恢复 6 0分钟后再观察 4小时 ;2内毒素 (L PS)组 (6只 ) :以 1.0 0～ 1.2 5μg/ kg L PS静注 ;3休克 L PS组 (6只 ) :低血容量性休克恢复 6 0分钟后再静注低剂量 L PS;4正常对照组 (4只 )。分别在休克前、休克 6 0分钟、休克恢复 6 0分钟、静注 L PS2和 4小时 5个点抽血测 IL 8、IL 1β、ICAM 1和 VCAM 1水平。结果 :休克 L PS组血浆 VCAM 1水平于注射 L PS4小时后显著高于正常对照组 (P<0 .0 5 ) ;血浆ICAM 1水平于注射内毒素第 2和 4小时后亦均高于正常对照组 (P均 <0 .0 5 ) ;休克组、休克 L PS组血浆IL 8浓度在注射 L PS后 2小时均显著高于正常对照组 (P均 <0 .0 5 ) ;休克组和休克 L PS组兔在休克期血浆 IL 1β浓度显著升高 ,而休克 L PS组于静注 1μg/ kg L PS后 2和 4小时 ,血浆 IL 1β浓度再次显著升高。结论 :低血容量性休克后再注射低剂量内毒素可导致血浆 ICAM 1和

The role of intercellular adhesion molecule1,vascular cell adhesion molecule1 and interleukin8 in early acute respiratory distress syndrome

Objective:To observe chan ges in plasma interleukin8(IL8),intercellular adhesion molecule1 (ICAM1),vascular cell adhesion molecule1(VCAM1) and their relationship to IL1β during he morrhagic shock followed by a lowdose lipopolysaccharide (LPS) chall enge.Methods:Twentytwo New Zealand rabbits were assigned to four groups.①In hemo rrhagic shock group,shock was sustained by reducing cardiac output (CO) to 40% of baseline for 60 minutes,then resuscitation was performed with shed blood and maintained CO near baseline with Ringer solution for 4 hours.②In LPS group,anima ls received intravenously 1.001.25 μg/kg LPS.③In hemorrhagics hock plus LPS group, animals were intravenously infused the same dose of LPS,lasting for 4 hours after resuscitation for 60 minutes.④Normal control group.Results:In shock plus LPS group,VCAM1 levels significantly increased at 4 ho urs following LPS infusion compared to normal controls (P<0.05).Also,plasm a ICAM1 levels markedly elevated at 2 and 4 hours after LPS challenge(both P<0.05).The IL1β levels,which sig nificantly increased after 60 minutes shock,were found in both shock plus LPS gr oup and shock only group(both P<0.05).Plasma IL8 levels in all four grou ps did not significantly change at different intervals,except the values at 2 hours postLPS infusion (both P<0.05) in shoc k only and shock plus LPS group.Plasma IL1β levels in shock group returned to normal range after resuscitation,while it maintained high values at 2 and 4 hours after LPS infusion in shock plus LPS group(both P<0.05).Conclusions:These data suggest that hemorrhagic shock followed by a lowdose LPS challenge can lead to the elevation of plasma ICAM1 and VCAM1 levels,which might play important roles in increasing pulmonary vascular permeability.