Total Parenteral Nutrition Causes Circumferential Intestinal Atrophy, Remodeling of the Intestinal Wall, and Redistribution of Eosinophils in the Rat Gastrointestinal Tract.

Summary, in English

Total parenteral nutrition (TPN) is held to cause intestinal atrophy and weaken mechanical and immunological barriers. To monitor the degree of atrophy caused by TPN, female Sprague-Dawley rats were, for 8 days, maintained on TPN (n = 6) and compared to identically housed controls given food and water ad libitum (n = 6). Specimens from jejunum, ileum, and colon were taken for histology and morphometric analysis. Topographic distribution and presence of eosinophils, by eosinophil peroxidase (EPO) staining, were examined in the gastric fundus, jejunum, ileum, and colon. Atrophy in terms of a markedly reduced circumference was noted throughout the intestinal tract in all rats subjected to TPN. The width of jejunal and ileal villi was narrowed and the length of jejunal villi was decreased. Furthermore, submucosal thickness in the jejunum and ileum increased. The height of ileal enterocytes remained unaltered. The number of goblet cells decreased in jejunal but not in ileal villi. The Paneth cells, suggested to play important roles in innate defense, increased in size. In the gastric fundus a marked increase in eosinophils was revealed predominantly in the mucosa and submucosa. The number and distribution of jejunal and ileal eosinophils were identical to those of controls. In colon from TPN rats, a redistribution of eosinophils was noted, causing a "band-like" accumulation of eosinophils in the basal portion of the mucosa. In conclusion, TPN causes gut atrophy and an increase in Paneth cell size. Eosinophils increase in number in the gastric fundus and a topographic redistribution occurs in the colon.

• Författare: Mikael Ekelund; Elin Sand; Mats Ekelund; Eva Ekblad
• Avdelning/ar: Neurogastroenterology; Kirurgi, Lund
• Publiceringsår: 2007
• Språk: Engelska
• Sidor: 1833-1839
• Publikation/Tidskrift/Serie: Digestive Diseases and Sciences
• Volym: 52
• Issue: 8
• Länkar: http://www.ncbi.nlm.nih.gov/pubmed/17390221; http://link.springer.com/article/10.1007%2Fs10620-006-9678-z; http://dx.doi.org/10.1007/s10620-006-9678-z
• Dokumenttyp: Artikel i tidskrift
• Förlag: Springer
• Ämne: Gastroenterology and Hepatology
• Status: Published
• Forskningsgrupp: Neurogastroenterology
• ISBN/ISSN/Övrigt: ISSN: 1573-2568