肠淋巴再灌注加重肠系膜上动脉闭塞性休克大鼠肺部炎症反应

Mesenteric Lymph Reperfusion Aggravates Pulmonary Inflammatory Response in Superior Mesenteric Artery Occlusion Shock Rats

目的:研究肠系膜淋巴再灌注对肠系膜上动脉闭塞性(SMAO)休克大鼠肺部炎症反应的影响。方法:24只Wistar雄性大鼠均分为4组:SMAO组,MLR组,SMAO+MLR组,SHAM组。再灌注2h后,迅速留取肺组织,一部分制备组织匀浆,检测细胞间粘附分子(ICAM-1)和晚期糖基化产物受体(RAGE)。再另外选取固定位置肺部组织放入中性甲醛中固定,用于测定肺内HMGB1、RAGE的表达。结果:SMAO与SMAO+MLR组肺部组织匀浆ICAM-1、RAGE含量显著高于MLR与SHAM组,且SMAO+MLR组肺组织匀浆的ICAM-1、RAGE含量高于SMAO组。肺部组织内HMGB1和RAGE在MLR组与SHAM组基本不表达,或少量表达,MLR加重了SMAO休克模型中HMGB1和RAGE的表达。结论:MLR加重SMAO休克大鼠肺部炎症反应,进一步证实肠淋巴途径在SMAO休克发病学中具有重要作用,同时证实HMGB1及RAGE在SMAO休克大鼠的炎症失常反应中起重要作用。

Objective： To investigate the effect of mesenteric lymph reperfusion on pulmonary inflammatory response in superior mesenteric artery occlusion （SMAO） shock rats. Methods： A total of 24 male Wistar rats were randomly divided into four groups： SMAO group, MLR group, SMAO＋MLR group, SHAM group. 2h after reperfusion, lung tissue were taken, part of which was homogenized for determining intercellular adhesion molecule-1 （ICAM-1） and the receptor of advanced glycation end-products （RAGE）; At the same time, some fixed lung tissue was fasten by neutral formalin for determining the activity of RAGE and high mobility group protein-1 （HMGB 1）. Results： The ICAM-1 and RAGE of lung tissue homogenate in SMAO and SMAO＋MLR group were higher than these in SHAM and MLR group, and these indexes in SMAO＋MLR group were significantly higher than those in SMAO group. HMGB 1 and RAGE of lung tissue in SHAM group and MLR group was rare. Mesenteric lymph reperfusion aggravated the expression of HMGB 1 and RAGE in SMAO shock model. Conclusion：Mesenteric lymph reperfusion aggravated pulmonary inflammatory response in superior mesenteric artery occlusion shock rats, which proved that mesenteric lymph way was crucial to the pathogencsis of SMAO shock. It also showed that HMGB 1 and RAGE may play a pivotal role in the pathogenesis of inflammatory disorders after SMAO shock rats.