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作 者:萧正伦[1] 黄海鹭[1] 徐远达[1] 罗炜[1]
出 处:《中国危重病急救医学》2000年第6期346-349,共4页Chinese Critical Care Medicine
基 金:广东省卫生厅科研基金!资助项目 (96 Z 5 84)
摘 要:目的 :观察急性失血致低血容量性休克后低剂量内毒素对血浆和肺泡灌洗液 ( BAL F)中前炎症细胞因子白介素 1β( IL 1β)和肿瘤坏死因子 α( TNFα)水平变化的影响。方法 :2 2只新西兰白兔分成 4组 :1低血容量性休克组 6只 :快速失血持续 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内毒素组 6只 :以 1μg/ kg的低剂量内毒素 ( L PS)静注 ;3休克加 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对照组 ( 4只 )。各组分别在休克前、休克 6 0分钟、休克恢复 6 0分钟、静注 L PS 2小时和 4小时 5个时间点抽血。结果 :休克组和休克加 L PS组动物休克期血浆 IL 1β水平有显著升高 ,休克恢复后回降正常 ;休克加 L PS组在静注 L PS后 2~ 4小时血浆 IL 1β浓度再次持续显著升高 ,且 BAL F中的 IL 1β浓度与对照组比较也有显著升高。而 TNFα水平除在 BAL F中有明显升高外 ,在各组动物实验中均未见显著改变。休克加 L PS组动物左肺干重与湿重比与对照组比较有显著差异 ( 0 .17± 0 .0 2比 0 .30± 0 .0 3)。结论 :前炎症细胞因子水平的升高提示短时的低血容量性休克可能启动了全身的炎症反应 ,增加了机体对低剂量 L PS产生炎性肺水肿的敏感性 ;Objective:To investigate the effects of lowdose endotoxin challenge on plasma and bronchoalveolar lavage fluid (BALF) tumor necrosis factorα(TNFα),interleukin1β(IL1β) levels in rabbits after hemorrhagic shock followed by resuscitation.Methods:22 New Zealand rabbits were assigned to four groups:hemorrhagic shock group ( n =6),endotoxin (1 μg/kg) group ( n =6),hemorrhagic shock plus endotoxin group ( n =6),and normal controls ( n =4).Hemorrhagic shock was sustained by reducing cardic output (CO) to 40% of baseline for 60 minutes,then resuscitated with shed blood and maintained CO as baseline with Ringer solution for 4 hours.After resuscitation of 60 minutes,1 μg/kg of endotoxin was infused intravenously.Results:Plasma IL1β levels increased in animals during shock period,and returned to normal value after resuscitation.Following infusion of lowdose endotoxin,plasma IL1β levels markedly elevated again at 24 hours,and IL1β levels in BALF were significantly higher compared with the controls.No marked changes in plasma TNFα levels were observed in these groups at any time point,while TNFα levels in BALF were significant higher in hemorrhagic shock plus endotoxin group and endotoxin group compared with control group.In addition,a significant difference in left pulmonary drytowet ratio was found between hemorrhagic shock plus endotoxin group and normal controls (0 17±0 02 vs.0 30±0 03).Conclusions:These data suggest that sustained elevation of IL1β rather than TNFα,induced by lowdose endotoxin challenge following acute hemorrhagic shock,may be of importance to increase the sensitivity of pulmonary vascular permeability.
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