Intestinal barrier damage caused by trauma and lipopolysaccharide

来源 :World Journal of Gastroenterology | 被引量 : 0次 | 上传用户:vergillove
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AIM:To investigate the intestinal barrier function damageinduced by trauma and infection in rats.METHODS:Experimental models of surgical trauma andinfection were established in rats.Adult Sprague-Dawleyrats were divided into 4 groups:control group (n=8),ENgroup (n=10),PN group (n=9) and Sep group (n=8).The rats in PN and Sep groups were made into PN modelsthat received isonitrogenous,isocaloric and isovolumic TPNsolution during the 7-d period.Rats in EN and Sep groupsreceived laparotomy and cervical catheterization on day1 and received lipopolysaccharide injection intraperitoneallyon d 7.On the 7~(th) day all the animals were garaged withlactulose and mannitol to test the intestinal permeability.Twenty-four hours later samples were collected and examined.RESULTS:The inflammatory responses became graduallyaggravated from EN group to Sep group.The mucosalstructure of small intestine was markedly impaired in PNand Sep groups.There was a low response in IgA level inSep group when compared with that of EN group.Lipopolysaccharide injection also increased the nitric oxidelevels in the plasma of the rats.The intestinal permeabilityand bacterial translocation increased significantly in Sepgroup compared with that of control group.CONCLUSION:One wk of parenteral nutrition causes anatrophy of the intestinal mucosa and results in a moderateinflammatory reaction in the rats.Endotoxemia aggravatsthe inflammatory responses that caused by laparotomyplus TPN,increases the production of nitric oxide in thebody,and damages the intestinal barrier function. AIM: To investigate the intestinal barrier function damage induced by trauma and infection in rats. METHODS: Experimental models of surgical trauma and infection were established in rats. Adult Sprague-Dawleyrats were divided into 4 groups: control group (n = 8), ENgroup PN 10 (n = 9) and Sep group (n = 8). The rats in PN and Sep groups were made into PN model stalled received isonitrogenous, isocaloric and isovolumic TPNsolution during the 7-d period. Rats in EN and Sep groupsreceived laparotomy and cervical catheterization on day1 and received lipopolysaccharide injection intraperitoneally on d 7.On the 7 ~ (th) day all the animals were garaged with lactul and mannitol to test the intestinal permeability.Twenty-four hours later samples were collected and examined .RESULTS : The inflammatory responses became gradually accumulated from EN group to Sep group. The mucosalstructure of small intestine was markedly impaired in PNand Sep groups. There was a low response in IgA level inSep group when compared with that of EN group. Lipopolysaccharide injection also increased the nitric oxide levels in the plasma of the rats. intestinal permeability and bacterial translocation increased significantly in Sepgroup compared with that of control group. CONCLUSION: One wk of parenteral nutrition causes anatrophy of the intestinal mucosa and results in a moderate inflammatory reaction in the rats. Endotoxemia aggravatsthe inflammatory responses that caused by laparotomyplus TPN, increases the production of nitric oxide in the body, and damages the intestinal barrier function.
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