Loss of the Intestinal Mucus Layer in the Normal Rat Causes Gut Injury But Not Toxic Mesenteric Lymph nor Lung Injury

• DOI: 10.1097/shk.0b013e3181dc3ff5
• Publication Date: 2010-03-23T06:46:57Z
• Authors: Susan M. Sharpe; Xiaofa Qin; Qi Lu; Eleonora Feketeova; David C. Palange; Wei Dong; Sharvil U. Sheth; Marlon A. Lee; Diego Reino; Da-Zhong Xu; Edwin A. Deitch
• Keywords: Male; 0303 health sciences; Acute Lung Injury; Models, Biological; Permeability; Acetylcysteine; Rats; Mucus; 03 medical and health sciences; Ileum; Bacterial Translocation; Animals; Mesentery; Lymph; Intestinal Mucosa; Hydrophobic and Hydrophilic Interactions; Ligation; Lung; Pancreas; Evans Blue; Expectorants; Peptide Hydrolases

There is substantial evidence that gut barrier failure associated with distant organ injury and systemic inflammation. After major trauma or stress, the factors mechanisms involved in are unknown. Our primary hypothesis loss of intestinal mucus layer will result normal exacerbated by presence luminal pancreatic proteases. secondary produced production biologically active mesenteric lymph consequently (i.e., lung) injury. To test this hypothesis, five groups rats were studied: 1) uninstrumented naive rats; 2) control which a ligated segment distal ileum was filled saline; 3) proteases placed their ileal segments; 4) mucolytic N-acetylcysteine (NAC) 5) exposed to NAC segments. The potential consequences induced assessed measuring biological activity as well gut-induced lung Exposure intestine NAC, but not saline proteases, led increased permeability, hydrophobicity, decrease layer, morphological villous Although themselves did cause injury, combination caused more severe than alone, suggesting once impaired, can injure now vulnerable gut. Because comparable levels insults mediated lymph, we next tested whether local model would produce lead It not, itself may be sufficient induce dysfunction. Therefore, especially intraluminal dysfunction otherwise