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Spantide对急性坏死性胰腺炎胰腺肠源性感染治疗作用的研究
作者:宿士智1 石欣2 高乃荣2 
单位:1.首都医科大学大兴医院,普外科一区,北京,102600; 2.东南大学附属中大医院,普外科,江苏,南京,210009
关键词:急性坏死性胰腺炎 神经激肽-1受体 P物质 肠系膜淋巴结 大鼠 Sprague-Dawley 
分类号:R657.5
出版年·卷·期(页码):2007·26·第一期(7-10)
摘要:

目的:研究P物质受体拮抗剂Spantide能否减少肠道细菌移位的发生﹑减轻胰腺肠源性感染并提高实验动物的生存率.方法:将健康成年SD大鼠随机分为对照组(24只)和实验组(再分为NS、P物质和Spantide 3组,每组34只).除实验组分别各取10只作48h死亡率观察外,余均于制模成功后8h和16h处死.取末端回肠行病理组织学评分;用放免γ计数器测定尿液中99m锝亚锡喷替酸(99mTc-DTPA)的脉冲数,计算肠黏膜通透性;取胰腺和末端回肠内容物作细菌培养.结果:Spantide组与NS组及P物质组比较,肠黏膜病理学改变明显减轻,胰腺细菌培养阳性率也明显降低(P<0.05).Spantide组48h死亡率明显低于其它两组(P<0.05).结论:使用P物质受体拮抗剂Spantide可明显减轻急性坏死性胰腺炎时胰腺肠源性感染的程度,提高实验大鼠的生存率.

Objective To investigate the effect of spantide,neurokinin-1 receptor(NK-1R)antagonist,on the intestinal originated infection of pancreas.Methods One hundred and twenty-six adult Sprague-Dawley rats were randomly divided into control group(n=24)and experimental group(n=102);the latter included 3 subgroups:ANP/NS group(n=34),ANP/Substance P(SP)group(n=34)and ANP/spantide group(n=34).The rats in control group received laparotomy only.Sacrifices were made 8h or 16h later in control group and experimental groups after induction respectively,except for 10 rats in each ANP group for the purpose of observation.The intestine was harvested for pathologic examination.Intestinal mucosal permeability was studied by measuring the radioactivities of 99mtechnetium diethlene triamine pentacetic acid(99mTc-DTPA)content in urinary.Pancreas and the content in ileum were obtained for bacteriological culture.Results In the ANP/NS and ANP/SP group,histological damages in intestinal mucosa and pancreas were observed at 8 h after induction,which deteriorated at 16 h after induction,with a significantly higher histology scores compared with that in the control group(P<0.05).As to the ANP/spantide group,the histological damages of intestine and pancreas were improved(P<0.05).The mortality of ANP/spantide group was significantly lower than that of group ANP/NS and group ANP/SP(P<0.05,respectively).Conclusion Spantide can protect mucous barrier,decrease the bacterial translocation and reduce the rats′ mortality.

参考文献:

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[4] 石欣, 高乃荣, 杨永久. 急性坏死性胰腺炎肠黏膜损害与NK-1R的过度表达相关. 中国病理生理杂志2003(8)
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