肝门阻断再灌注致脑皮层血管内皮损伤中TNF-α和IL-10的变化

目的观察肝门阻断再灌注(HPO)对脑皮层血管内皮的损伤并探讨可能机制。方法 32只大鼠随机分成Sham组和HPO组(均n=16),分别建立假手术、肝门阻断再灌注模型,以脑血管内皮和小肠黏膜为目标,采用干湿重法比较脑水肿程度、伊文思兰比较BBB渗透率、光电镜研究组织和超微结构损害、血气分析测定电解质、酸碱平衡以及放免法测定血浆TNF-α、IL-10浓度等,探索HPO再灌注对肠黏膜和脑血管内皮的作用和机制。结果①肠损伤Chiu’评分HPO组>Sham组(312±42vs30±11,P<0.01)。②光、电镜下HPO组脑皮层血管内皮损伤,间质水肿,胶质细胞变性,血管周围神经突起水肿。③HPO组见BBB通透性增加,有脑水肿倾向。④HPO组TNF-α、IL-10浓度以及K+]和Ca2+]明显高于Sham组(均P<0.05),并有酸血症。结论肝门阻断再灌注后肠损伤是导致脑皮层血管内皮损伤的主要因素,TNF-α刺激肠PMN浸润产生的伤害因子通过血液和循环系统传递引起脑皮层等远隔脏器的继发损害。

The damages of cortex vascular endothelial undergone hepatic portal occlusion and the change of TNF-α和L-10

Objective To observe the BBB damages undergone hepatic portal occlusion(HPO)in vivo and explored the mechanisms of TNF-αand IL-10.Methods In the research the Pringle’ measure was used to install HPO model without bypass in rats and observed the subsequent brain cortex pathological changes and BBB permeability.The morphology were studied by electron microscope and light microscope,MPO measurement test PMN infiltration level in intestine,and also test the concentration of TNF-α、IL-10、K+、Ca2+and pH in plasma.Results ①The Chiu’ scores in Group HPO,Group Sham were 312±42 vs 30±11 respectively.The intestine PMN infiltration in Group HPO were more serious than Group Sham.②The cerebral vascular endothelial injury,gliocytes degeneration,nerve edema around demaged vessels were observed in Group HPO,but in Group sham all were normal.③ The BBB permeability in Group HPO were increased and show brain edema tendency.④ The concentration of TNF-α、IL-10、K+、Ca2+ in Group HPO were obviously higher than those in Group Sham(all P<0.05).Conclusion Intestine were serious injuried undergone HPO reperfusion and TNF-α irrated PMN infiltrated.These were the main causes of BBB permeability increased and brain edema.