The effect of sennosides on bacterial translocation and survival in a model of acute hemorrhagic pancreatitis
The effect of sennosides on bacterial translocation and survival in a model of acute hemorrhagic pancreatitis
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DOI：
10.1097/00006676-199901000-00006
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发表时间：
1999-01-01
期刊：
影响因子：
2.9
通讯作者：
Alexandre, JW
中科院分区：
文献类型：
--
作者：
Chen, XL;Valente, JF;Alexandre, JW
细菌移位导致随后的感染并发症是急性出血性胰腺炎（AHP）预后的重要决定因素。结肠梗阻和肠屏障功能受损，往往伴随AHP可能易患易位。番泻苷是一种天然存在的泻药和利胆剂，刺激肠道粘液分泌，并具有有效的促进作用。在大鼠AHP模型中研究番泻苷诱导的肠道运动和分泌功能对细菌移位和存活的影响。用2%脱氧胆酸钠（DCA，0.4ml/kg）胰管内注射诱导大鼠重症急性胰腺炎模型。假手术组（A组）导管内注射生理盐水，B组（B组）灌胃蒸馏水，C组灌胃番泻苷溶液，每8 h 1次。48小时后，异硫氰酸荧光素标记的葡聚糖，血清内毒素和淀粉酶水平，肠道转运和细菌易位到肠系膜淋巴结（MLN）和胰腺组织进行了测定。取胰腺和肠进行组织学研究。所有A组动物均存活，未发生胰腺炎或内毒素血症，而B和C组均显示重度出血性胰腺炎伴坏死迹象。B组48 h死亡率为55%，C组为12.5%。在B组和C组大鼠中，分别观察到40%和20%的肠运动抑制，内毒素水平分别为61.36 +/- 28.26 pg/L和5.41 +/- 3.58 pg/L（p < 0.001）。胰腺组织和MLN培养物在100%的B组存活者和14%的C组存活者中呈阳性（p < 0.05）。C组动物的肠道组织学检查显示粘液分泌增加、杯状细胞增殖和肠细胞快速更新/更新的证据。在大鼠急性出血性胰腺炎模型中，用泻药番泻苷治疗可减少内毒素和细菌的移位，恢复肠动力，增加粘液分泌，并降低死亡率。其他泻药可能具有类似的性质，可能有助于预防急性胰腺炎的感染性并发症。
Bacterial translocation leading to subsequent infectious complications is a significant determinant of outcome in acute hemorrhagic pancreatitis (AHP). The colonic ileus and impaired intestinal barrier function that often accompany AHP may predispose to translocation. Sennoside is a naturally occurring cathartic and choleretic agent that stimulates intestinal mucous secretion and has potent promotility effects. The impact of sennoside-induced intestinal motility and secretory function on bacterial translocation and survival was studied in a rat model of AHP. Severe acute pancreatitis was induced in rats by the intraductal infusion of 2% sodium deoxycholate (DCA, 0.4 ml/kg). A group of sham-operated rats (group A) received intraductal saline, whereas experimental animals were subsequently administered distilled water (group B) or sennoside solution (group C) by gavage every 8 h. After 48 h, intestinal transit of fluorescein isothiocyanate-labeled dextran, serum endotoxin, and amylase levels, and bacterial translocation to mesenteric lymph nodes (MLNs) and pancreatic tissue were determined. The pancreas and intestine were sampled for histologic study. All group A animals survived and did not develop pancreatitis or endotoxemia, whereas groups B and C all demonstrated severe hemorrhagic pancreatitis with evidence of necrosis. Mortality at 48 h was 55% in group B versus 12.5% in group C. Inhibition of intestinal motility was noted in 40% versus 20%, and endotoxin levels were 61.36 +/- 28.26 pg/L versus 5.41 +/- 3.58 pg/L in group B versus group C rats, respectively (p < 0.001). Pancreatic tissue and MLN cultures were positive in 100% of group B survivors versus 14% of group C survivors (p < 0.05). Histologic examination of the intestine in group C animals showed increased mucous secretion, proliferation of goblet cells, and evidence of rapid turnover/renewal of enterocytes. Treatment with the cathartic agent, sennoside, reduced translocation of endotoxin and bacteria, restored intestinal motility, increased mucous secretion, and reduced mortality in a model of acute hemorrhagic pancreatitis in the rat. Other cathartics may have similar properties and may be useful in preventing infectious complications in acute pancreatitis.