摘要
目的建立猪急性重症胰腺炎(ASP)模型,并观察 ASP 后肠源性内毒素/细菌的易位。方法选健康长白种猪40头,体重17～22kg,雌雄不限,随机分为 ASP 组(n=34)和对照组(n=6)。在麻醉状态下,进腹向胰总管内注入1ml/kg 5%牛磺胆酸钠混合液(内含8000～10000BAEE 单位胰蛋白酶/ml,pH7.6)诱导 ASP。以0.9%NaCl 磷酸盐缓冲液取代5%牛磺胆酸钠混合液即为对照组。采集腔静脉血作内毒素测定(鲎试剂法)。ASP 后72小时,采集门、腔静脉作系列细菌定量培养和细菌鉴定。然后推注10%氯化钾20ml 处死后立即进胸腹取大小肠系膜淋巴结、肺组织、肺门淋巴结、胰组织,称重后研磨成组织匀浆,并作细菌定量培养和细菌鉴定。结果血浆内毒素水平 ASP 后6h 明显升高,48h 达峰值(P均<0.01)。ASP后72h,在门、腔静脉、肺门淋巴结、大小肠系膜淋巴结、肺及胰腺组织中出现大量易位细菌。结论 (1)成功地建立了猪 ASP模型;(2)ASP 后早期出现血浆内毒素水平明显升高,最大可能系肠道内毒素易位所致;(3)ASP 后72h 在门、腔静脉血和肠道远离器官和组织中可出现大量易位细菌。
Objective To set up a model of acute severe pancreatitis(ASP)in pigs and to observe its relationship to the gut-originated bacterial/endotoxin translocation.Methods There were forty pigs weighing 17～22kg,which were divided into two groups.Anesthesized pigs were subjected ASP(n=34)induced by injecting 1ml/kg of combined solution of 5% sodium taurocholate and 8000～10000 BAEE units trypsin/ml into pancreas via pancreatic duct,and sham-ASP(n=6)for control.Systemic plasma endotoxin levels was quantified by the chromogenic limulus amebocyte lysate(LAL)technique.Both portal and systemic blood samples were collected before and 72 hours after the induction of ASP and cultured for aerobic as well as anaerobic bacterial growth.Subsequently,All pigs were sacrificed by injecting 20ml of 10% KCL intravenously.Specimens of tissue from mesenteriolum and mesocolon lymph nodes,lung,pulmonary portal lymph nodes and pancreas were removed,weighed and homogenized in grinding tubes.Aliquots of the homogenate were cultured as blood mentioned above.Positive specimens were subcultured and the bacteria identified by standard procedure.Results Systemic plasma endotoxin levels increased rapidly 6 hours following the induction of ASP,reaching a peak value 48 hours later(P<0.01).The magnitude of bacterial translocation to portal and systemic blood and the systemic organs occurred 72 hours following the induction of ASP.Conclusions(1)A model of acute severe pancreatitis was set up in pigs;(2)Early endotoxemia following ASP might mostly be associated with the gut-originated endotoxin translocation;(3)The magnitude of bacterial translocation to the portal and systemic blood and the remote systemic organs following the induction of ASP was mentioned.
