摘要
目的:探讨肠源性内毒素 (endotoxin,ET)及血浆肿瘤坏死因子 - α(TNF- α)在油酸所致急性呼吸窘迫综合征 (ARDS)过程所继发的肺外器官损害中的动态变化及其作用。 方法:将 34只成年家兔随机分组 ,其中 6只作为对照组 ,另外 2 8只从耳缘静脉缓慢注入油酸 (OA) 0 .1mg/kg,以 30、6 0、90、12 0 m in为时限又分为 4组作为实验组 ,监测平均动脉血压 (MABP)、血气及门静脉、腔静脉血浆 ET、TNF- α的动态变化。同时对小肠组织进行光镜及电镜观察。 结果 :实验组注射 OA6 0 m in后 ,门静脉血浆 ET水平显著高于对照组 (P <0 .0 1) ,而腔静脉中的ET在注射 OA90 min后显著高于对照组 (P <0 .0 5～ 0 .0 1) ,且 OA6 0 min与 OA90 min时限的门静脉血浆 ET水平与同时点的腔静脉血浆 ET水平相比差异具有统计学意义。实验组注射 OA6 0 m in后门、腔静脉血浆 TNF- α水平显著高于对照组 (P <0 .0 5～ 0 .0 1) ,门静脉血浆 TNF- α水平在注射 OA90 m in后达高峰。电镜下可见 OA6 0、90 m in组小肠微绒毛排列紊乱 ,线粒体肿胀 ,粗面内质网扩张 ,上述改变在 OA12 0 min组加重。结论 :在 OA致 ARDS过程中 ,有肠源性 ET血症的发生及 TNF- α的过量释放 ,它们可能参与 OA所致
Objective: To investigate the potential role of gut derived endotoxin (ET) and changes of plasma tumor necrosis factor α (TNF α) during oleic acid induced acute lung injury. Methods: 34 rabbits were randomly divided into control group (n=6) and experimental group (n=28). The experimental group was divided into 4 groups of OA30 min, OA60 min, OA90 min and OA120 min after injection of OA (0.1 ml/kg) into ear vein slowly. Developing changes of MABP and blood gas, levels of ET in portal and in systemic circulation were measured. Results: Compared with the control group, plasma levels of ET in portal circulation of experimental group were significantly increased after OA60 min (P<0.01), but plasma levels of ET in systemic circulation were markedly increased after OA90 min (P<0.05). After OA90 min, plasma TNF α in systemic circulation and in portal circulation were found to be markedly elevated in experimental group (P<0.05) and TNF α peaked in portal systemic at 90 minutes. The levels of plasma TNF α were positively correlated with the level of plasma ET. under the electron microscope, the villi of intestine were disarranged to a greater or lesser degree; mitochondria swelled; rough surfaced endoplasmic reticulum enlarged in OA60 min group and OA90 min group. Conclusion: These results suggest that oleic acid induced acute lung injury may lead obvious gu derived endotoxemia and over production of TNF α.
出处
《新疆医科大学学报》
CAS
2003年第3期233-235,共3页
Journal of Xinjiang Medical University
