Li L L, Zhang C H, Liu J C, Yang L N, Niu C Y, Zhao Z G
Institute of Microcirculation, Hebei North University, Zhangjiakou, Hebei, China.
Braz J Med Biol Res. 2014 May;47(5):376-83. doi: 10.1590/1414-431x20143639. Epub 2014 May 2.
The intestinal lymph pathway plays an important role in the pathogenesis of organ injury following superior mesenteric artery occlusion (SMAO) shock. We hypothesized that mesenteric lymph reperfusion (MLR) is a major cause of spleen injury after SMAO shock. To test this hypothesis, SMAO shock was induced in Wistar rats by clamping the superior mesenteric artery (SMA) for 1 h, followed by reperfusion for 2 h. Similarly, MLR was performed by clamping the mesenteric lymph duct (MLD) for 1 h, followed by reperfusion for 2 h. In the MLR+SMAO group rats, both the SMA and MLD were clamped and then released for reperfusion for 2 h. SMAO shock alone elicited: 1) splenic structure injury, 2) increased levels of malondialdehyde, nitric oxide (NO), intercellular adhesion molecule-1, endotoxin, lipopolysaccharide receptor (CD14), lipopolysaccharide-binding protein, and tumor necrosis factor-α, 3) enhanced activities of NO synthase and myeloperoxidase, and 4) decreased activities of superoxide dismutase and ATPase. MLR following SMAO shock further aggravated these deleterious effects. We conclude that MLR exacerbates spleen injury caused by SMAO shock, which itself is associated with oxidative stress, excessive release of NO, recruitment of polymorphonuclear neutrophils, endotoxin translocation, and enhanced inflammatory responses.
肠淋巴途径在肠系膜上动脉闭塞（SMAO）休克后器官损伤的发病机制中起重要作用。我们假设肠系膜淋巴再灌注（MLR）是SMAO休克后脾脏损伤的主要原因。为验证这一假设，通过夹闭Wistar大鼠的肠系膜上动脉（SMA）1小时，随后再灌注2小时，诱导SMAO休克。同样，通过夹闭肠系膜淋巴管（MLD）1小时，随后再灌注2小时来进行MLR。在MLR + SMAO组大鼠中，同时夹闭SMA和MLD，然后松开进行2小时的再灌注。单独的SMAO休克引发：1）脾脏结构损伤；2）丙二醛、一氧化氮（NO）、细胞间黏附分子-1、内毒素、脂多糖受体（CD14）、脂多糖结合蛋白和肿瘤坏死因子-α水平升高；3）NO合酶和髓过氧化物酶活性增强；4）超氧化物歧化酶和ATP酶活性降低。SMAO休克后的MLR进一步加重了这些有害影响。我们得出结论，MLR加剧了SMAO休克引起的脾脏损伤，而SMAO休克本身与氧化应激、NO过度释放、多形核中性粒细胞募集、内毒素移位及炎症反应增强有关。
