摘要
目的 观察重症急性坏死性胰腺炎(SAP)大鼠肠壁、肝脏和肺组织中免疫单核吞噬细胞分布的变化,并探讨谷氨酰胺对其的调节作用。方法 SD大鼠54只,随机分3组:假手术组(SO,n=18);SAP组(SAP,n=18);SAP谷氨酰胺治疗组(GLN,n=18)。采用5%牛磺胆酸钠溶液胆胰管内逆行注射诱导大鼠SAP模型。大鼠中心静脉置管,微量输液泵输注含等氮、等热卡的氨基酸溶液,GLN组加入3%丙氨酸-谷氨酰胺双肽(相当于2%谷氨酰胺溶液,剂量0.5g.kg-1·d-1)。术后24h、48h、72h分批处死大鼠并留取标本,分别采用鲎试剂比色法及免疫组化法测定血浆内毒素水平、肠上皮淋巴细胞、肝脏和肺单核吞噬细胞分布的变化。结果 血浆内毒素在SAP组明显高于SO组(P<0.05),且随着时间延长而递升;GLN治疗组血浆内毒素较SAP组显著下降(P<0.05)。SAP组肠上皮中淋巴细胞数较SO组明显减少(P<0.05);GLN治疗组则较SAP组明显上升(P<0.05)。溶菌酶组织化学染色显示,SO组肝脏和肺脏中单核吞噬细胞呈散在分布;而SAP组中单核吞噬细胞聚集成团,以术后24h最为显著;GLN治疗组阳性染色细胞聚集状态减弱。结论 肠道局部免疫功能的变化及由于内毒素等物质刺激而导致的肝、肺单核吞噬细胞过度活化促进了SAP的进一步发展。谷氨酰胺通过调节肠道局部。
Objective To observe the changes of immunocytes and macrophages in gut, liver and lung in rats with severe acute pancreatitis (SAP) and the effect of glutamine on these changes. Methods Fifty-four SD rats were randomly divided into 3 groups; sham operation group(SO, n=18), SAP group (n=18), and GLN group (SAP rats treated with Glutamine, n=18). The SAP model was induced by injection of 5% sterile sodium taurocholate solution into the bili-pancreatic duct. Isocaloric and isonitrogenous amino acid solution was infused continuously to the rats by a mini-pump via a central intravenous line. The rats in GLN group received 3% glutamine dipeptide solution (equivalent to 2% glutamine) with a dosage of 0. 5 g ·kg-1·d-1. The rats were sacrificed at 24 h, 48 h and 72 h after operation. Endotoxin in portal vein, and CD3+, CD4+, CD8+ lymphocytes in intestinal mucosa and macrophages in liver and lung were determined by immunohistochemistry methods. Results The endotoxin concentration was increased significantly in SAP group in a time-dependent manner (P< 0. 05. vs SO group), while glutamine decreased the endotoxin significantly (P<0. 05). The number of CD3+, CD4+, CD8+ lymphocytes was decreased in SAP group(P<0. 05, vs SO group) and increased in GLN group(P<0. 05, vs SAP group). The macrophages in the liver and lungs were accumulated in SAP group, especially at 24 h after the operation, but disappeared in glutamine treated rats. Conclusions The immunocytes dysfunction in the gut and the over-activation of macrophages in the liver and lungs are implicated in the development of SIRS in the setting of SAP. Glutamine protected the intestinal immune barrier, prevented endotoxin translocation and inhibited excessive activation of macrophages.
出处
《胰腺病学》
2002年第1期17-19,共3页
Chinese JOurnal of Pancreatology
基金
上海市科技启明星培养计划基金(No 99QB14009)