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作 者:范华[1] 谭庆华[1] 许兰涛[1] 吴浩[1] 黄明慧[1] 胡兵[1] 唐承薇[1]
机构地区:[1]四川大学华西医院人类疾病相关多肽研究室,成都610041
出 处:《中华消化杂志》2007年第2期99-102,共4页Chinese Journal of Digestion
基 金:国家自然基金项目资助(30330270)
摘 要:目的探讨肠缺血再灌注(IIR)后猕猴肠道菌群变化的原因。方法将10只健康成年猕猴分为对照组和IIR组,每组各5只。IIR组肠系膜上动脉夹闭60min,松解再灌注24h,造成缺血再灌注损伤。对照组行假手术。观察动物肠道大体形态改变,测定胃pH值;细菌培养分析回肠菌群的变化;免疫组化定位测定回肠局部胃肠多肽的分布,并用放射免疫分析法定量测定其水平变化,并在体外将胃肠多肽与肠道细菌共同孵育,观察两者有无相互作用。结果猕猴IIR损伤后,回肠内细菌较正常增加约10^6倍,以大肠杆菌等需氧菌为优势菌群;小肠明显充血扩张;胃内pH值由2.80±0.84增至7.20±0.84,伴有胆汁反流;全回肠组织中胃肠多肽(生长抑素、血管活性肠肽、P物质)明显增加,而黏膜中生长抑素及血管活性肠肽的浓度却减少;胃肠多肽与肠道细菌共同培养后,胃肠多肽的含量及细菌数量均无明显变化。结论猕猴IIR后,小肠细菌过度生长可能由小肠动力降低直接或间接导致。小肠肌间神经丛中的生长抑素及血管活性肠肽增加可能是此刻小肠动力降低的启动因素。Objective To investigate the factors involved in the alterations of the intestinal microflora after intestinal ischemia reperfusion (IIR) in macaque. The effects of gastrointestinal peptides on the intestinal microflora were also studied. Methods Ten macaques were divided into control and IIR groups of 5 each. The IIR injury was induced by clamping superior mesenteric artery for 60 min, followed by reperfusion of 24 hrs. The control group received sham surgery. The morphology of the intestine was observed. The gastric pH and the alteration of ileal microflora were measured. The distri- bution of gastro intestinal polypeptides in the ileum was visualized by immunohistoehemistry and was quantified by radioimmunoassay. Gastro intestinal polypeptides and intestinal bacteria were co-incubated in vitro to test the possible interaction between them. Results The amount of bacteria in the macaque ileum after IIR was 106 folds higher than that in normal control, with predominant of E. coli and other aerobic bacteria. There was significant dilation and congestion of the small intestine after IIR. Gastric pH was increased from 2.80 ± 0.84 to 7.20±0.84 with bile reflux into the stomach. The expressions of somatostatin(SST), vasoactive intestinal peptide (VIP), substance P in whole ileum tissue were increased significantly. However, the concentrations of SST and VIP in mucosal layer were signicantly decreased. Neither gut peptides nor intestinal bacteria were altered significantly after co-incubation. Conclusions Intestinal bacterial overgrowth after IIR may be the direct or indirect results of intestinal motility dysfunction. The increased SST and VIP in the intra-muscular neural plexus of the small intestine may be the initialing factor of reduced intestinal motility.
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