摘要
目的 探讨重症急性胰腺炎 (SAP)时血浆细胞因子与肠道屏障损害后肠源性细菌和内毒素移位的关系。方法 将SD大鼠 (清洁级 ) 72只随机分为假手术组 (n =3 6)和SAP组 (n =3 6)。采用胰管内逆行注射 4%牛磺胆酸钠溶液的方法制作SAP模型。观察胰腺和回肠的病理改变 ,动态测定血浆TNF -α、IL -6、IL -10和DAO活性、LPS水平以及腹腔脏器细菌移位率。结果 制模后血浆TNF -α、IL -6水平明显升高 ,48h达到高峰 ,IL -10 6h后才明显升高 ;血浆DAO活性早期升高 ,2 4h后明显降低 ;LPS水平早期即有明显升高 ,48h达到高峰 ;SAP 2 4h脏器细菌移位率明显升高 ,72h达到 5 8 3 %。结论 SAP早期即有细胞因子水平的升高和肠道屏障的损害 ,细胞因子通过损害肠道屏障 ,引起肠源性细菌和内毒素移位 ;同时 ,肠源性细菌和内毒素移位又促进细胞因子的大量释放 ,加重肠黏膜屏障本身的损害 ,造成恶性循环 ,引起SIRS和MODS的发生 。
Objective To investigate the relationship between the plasma cytokines and the translocation of intestinal bacteria and endotoxin after gut barrier injury in severe acute pancreatitis (SAP) rats. Methods SD rats were divided randomly into sham operation group(n=36) and SAP group (n=36). The rat model of SAP was set up by retrograde injection of 4% sodium taurocholate in biliopancreatic duct. Morphological changes of pancreas and ileum were observed. The plasma levels of TNF-a,IL-6 and IL-10 were determined by ELISA. The plasma levels of DAO activities and LPS were measured at various time points. The rates of bacterial translocation to abdominal organs were also calculated. Results The plasma levels of TNF-a and IL-6 obviously elevated immediately after SAP induction and reached peak value at 48 hours, and the plasma IL-10 level significantly increased only 6 hours after SAP induction. Plasma DAO activities increased at the early stage of SAP and obviously decreased at 24 hours. Plasma LPS levels also increased significantly at the early stage of SAP and reached peak value at 48 hours. The rates of bacterial translocation to organs sharply increased 24 hours after SAP induction and reached 58.3% at 72 hours. Conclusion The levels of cytokines increased and gut barrier function was injured in the early stage of SAP. Cytokines may impair the intestinal microcirculation and gut barrier function, which could promote the intestinal bacteria and endotoxin translocation. Simultaneously, intestinal bacteria-endotoxin translocation could also induce excessive release of cytokines and aggravate the gut barrier damage, which might cause systemic inflammatory response syndrome and multiple organ disfunction syndrome. There was a close relationship beween cytokines and the translocation of intestinal bacteria and endotoxin in SAP.
出处
《中国医师杂志》
CAS
2004年第8期1051-1054,共4页
Journal of Chinese Physician
