Cicalese L, Sahai A, Sileri P, Rastellini C, Subbotin V, Ford H, Lee K
Division of Transplant Surgery, University of Illinois at Chicago, 60612, USA.
Dig Dis Sci. 2001 May;46(5):1127-32. doi: 10.1023/a:1010786701289.
Infectious complications are the most frequent and severe complications of acute narcotizing pancreatitis (AP) with a mortality rate up to 80%. Although experimental and clinical studies suggest that the microbiologic source of pancreatic infection could be enteric, information in this regard is scant. This study evaluated bacterial translocation (BT) using mild and severe models of AP. Mild AP was induced by 6-hr continuous intravenous infusion of cerulein, while severe AP was induced by additional infusion of glycodeoxycholic acid into the biliopancreatic duct. BT was evaluated with organ cultures performed when animals were killed (24 hr). To confirm the gastrointestinal origin of the translocating microorganisms, fluorescent microspheres were also given to the animals in drinking water 24 hr before induction of AP. At the time of death beads were counted with a (fluorescence-activated cell sorter) (FACS) in peritoneal lavages and with fluorescent microscopy in frozen sections of the pancreata. Morphology of the distal small bowel showed significant changes in the animals with AP compared to controls, such as reduction of villus high and altered microvasculature. Mild AP induced BT to the pancreas in 100% of the animals, compared to pancreata from control groups. Severe AP induced increased BT to the pancreas. BT to liver and spleen was also significantly increased with AP. The presence of fluorescent microspheres confirmed their enteric derivation. This study provides evidence for the enteric origin of microorganisms responsible for pancreatic infectious complications during AP. The evidence of BT after laparotomy suggests an increased risk of infections with the association of these conditions. This could provide an explanation for the high mortality associated with laparotomy in course of AP.
感染性并发症是急性坏死性胰腺炎(AP)最常见且最严重的并发症,死亡率高达80%。尽管实验和临床研究表明胰腺感染的微生物来源可能是肠道,但这方面的信息却很少。本研究使用轻度和重度AP模型评估细菌移位(BT)。轻度AP通过连续6小时静脉输注雨蛙素诱导,而重度AP通过向胆胰管额外输注甘氨脱氧胆酸诱导。在动物处死时(24小时)通过器官培养评估BT。为了证实移位微生物的胃肠道来源,在诱导AP前24小时也给动物饮用含荧光微球的水。在死亡时,通过(荧光激活细胞分选仪)(FACS)对腹腔灌洗液中的珠子进行计数,并通过荧光显微镜对胰腺冰冻切片中的珠子进行计数。与对照组相比,AP动物的远端小肠形态有显著变化,如绒毛高度降低和微血管改变。与对照组胰腺相比,轻度AP在100%的动物中诱导了BT至胰腺。重度AP诱导BT至胰腺增加。AP时BT至肝脏和脾脏也显著增加。荧光微球的存在证实了它们的肠道来源。本研究为AP期间导致胰腺感染性并发症的微生物的肠道来源提供了证据。剖腹手术后BT的证据表明这些情况联合时感染风险增加。这可以解释AP病程中与剖腹手术相关的高死亡率。