Zhao Zi-gang, Yang Li-na, Zhao Yong-quan, Niu Chun-yu
Institute of Microcirculation, Hebei North University, Zhangjiakou, China.
Acta Cir Bras. 2014 Jun;29(6):359-64. doi: 10.1590/s0102-86502014000600002.
To determine the role of mesenteric lymph reperfusion (MLR) on endotoxin translocation in brain to discuss the mechanism of brain injury subjected to superior mesenteric artery occlusion (SMAO) shock.
Twenty-four rats were randomly assigned to MLR, SMAO, MLR+SMAO and sham groups. MLR was performed by clamping the mesenteric lymph duct (MLD) for 1 h and then allowing reperfusion for 2 h in the MLR group; SMAO involved clamping the superior mesenteric artery (SMA) for 1 h, followed by reperfusion for 2 h in the SMAO group; occlusion of both the SMA and MLD for 1 h was followed by reperfusion for 2 h in the MLR+SMAO group rats.
SMAO shock induced severe increased levels of the endotoxin, lipopolysaccharide receptor, lipopolysaccharide-binding protein, intercellular adhesion molecule-1 and tumor necrosis factor-α. Concurrently, MLR after SMAO shock further aggravates these deleterious effects.
Mesenteric lymph reperfusion exacerbated the endotoxin translocation in brain; thereby increased inflammatory response occurred, suggesting that the intestinal lymph pathway plays an important role in the brain injury after superior mesenteric artery occlusion shock.
确定肠系膜淋巴再灌注（MLR）在脑内毒素移位中的作用，以探讨肠系膜上动脉闭塞（SMAO）休克所致脑损伤的机制。
将24只大鼠随机分为MLR组、SMAO组、MLR+SMAO组和假手术组。MLR组通过夹闭肠系膜淋巴管（MLD）1小时，然后再灌注2小时来进行；SMAO组包括夹闭肠系膜上动脉（SMA）1小时，随后在SMAO组再灌注2小时；在MLR+SMAO组大鼠中，夹闭SMA和MLD 1小时后再灌注2小时。
SMAO休克导致内毒素、脂多糖受体、脂多糖结合蛋白、细胞间黏附分子-1和肿瘤坏死因子-α水平严重升高。同时，SMAO休克后的MLR进一步加重了这些有害影响。
肠系膜淋巴再灌注加剧了脑内毒素移位；从而导致炎症反应增加，提示肠道淋巴途径在肠系膜上动脉闭塞性休克后脑损伤中起重要作用。
