脓毒症大鼠小肠功能变化的研究

目的　探讨脓毒症大鼠小肠屏障、吸收、通透及其蠕动功能的变化。方法　以 Wistar大鼠缺血再灌注复合内毒素血症制备动物模型。将动物随机分为正常对照 ( N)、肠系膜上动脉夹闭 1h后再灌注 1h( I/ R1)、2 h( I/ R2 )和 4 h( I/ R4 )以及再灌注 2 h后复合内毒素 2 h( I/ RL)共 5个组。分别测定各组动物血或小肠组织二胺氧化酶 ( DAO)、D 乳酸、D 木糖水平及肠蠕动 ,同时进行小肠普通光镜检查。结果　 I/ R1、I/ R4和 I/ RL组血浆 DAO活性均显著升高 ( P均 <0 .0 5 ) ,小肠组织 DAO在 I/ R2和 I/ RL 组均显著降低( P均 <0 .0 5 ) ,从 N、I/ R1、I/ R2、I/ R4到 I/ RL,各组血浆 DAO和小肠 DAO的相关分析可见呈高度负相关( r= 0 .90 9,P<0 .0 0 1) ;I/ R 1、I/ R 2和 I/ RL组血浆 D乳酸均显著升高 ( P均 <0 .0 5 ) ;与 N组比较各组肠传输速度显著加快 ( P均 <0 .0 5 ) ;I/ R 1和 I/ RL组血中 D木糖浓度较 N组高 ,3h后仍高于 N组 ;血 DAO浓度与血 D乳酸浓度变化相关 ( r=0 .5 5 9,P<0 .0 5 )。结论　缺血再灌注后小肠的屏障、吸收、通透和蠕动功能均有不同程度的改变 ;缺血再灌注复合内毒素血症时再次加速或加重了小肠屏障、吸收、通透和传输功能的变化

Change in intestinal function in sepsis in rat

OBJECTIVE: To study the barrier function, absorption, permeability and peristalsis of intestine in sepsis in rats. METHODS: A Wistar rat model of sepsis was reproduced by ischemia/reperfusion (I/R) of the intestine combined with endotoxin challenge. Animal were randomly divided into normal, I/R 1 hours (I/R 1), I/R 2 hours (I/R 2), I/R 4 hours (I/R 4) and I/RL groups. The following parameters were measured in the experiments: (1) diamin oxidase activity (DAO), D-lactate and D-xylose levels in blood using spectrophotometry; (2) transit function of small intestine; (3) pathological examination of small intestine by light microscope. RESULTS: The results showed that plasma DAO activity was increased in I/R 1, I/R 4 and I/RL (all P<0.05), and small intestinal tissue DAO was decreased in I/R 2 and I/RL (both P<0.05). Negative correlations were found between plasma and intestinal DAO (r=-0.909, P<0.001). Plasma D-lactate was elevated significantly in I/R 1, I/R 2, and I/RL (all P<0.05). D-xylose content was increased at I/R1 and I/RL groups (both P<0.05), and it was significantly higher than controls at 3 hours. Similarly, a positive correlation was found between plasma DAO activity and plasma D-lactate level (r=0.559, P<0.05). CONCLUSION: The intestinal barrier function, absorption function, permeability, and transit are impaired after gut ischemia/reperfusion combined with endotoxin challenge.