The inflammation in the gut after experimental subarachnoid hemorrhage

J Surg Res. 2007 Jan;137(1):103-8. doi: 10.1016/j.jss.2006.06.023. Epub 2006 Oct 27.

Abstract

Background: Gastrointestinal dysfunction could be frequently observed in the patients suffering from SAH. This study test the hypothesis that experimental SAH could induce histopathological changes and inflammatory response associating with NF-kappaB activation pathway in the gut.

Materials and methods: A total of 17 rabbits were randomly divided into two groups: control group (n = 8) and SAH group (n = 9). In the SAH group, the animals were subjected to experimental SAH according to the "two-hemorrhage" method. The histopathological study was performed to detect the intestinal mucosal morphological changes and immunohistochemical study was used to detect the TNF-alpha and ICAM-1 expressions. NF-kappaB binding activity was measured using the electrophoretic mobility shift assay.

Results: It was demonstrated that some damage changes and leukocytes infiltration occurred in the intestinal mucosa after SAH. More positive cells for TNF-alpha and ICAM-1 were observed in the SAH group. The NF-kappaB binding activity in the intestines was significantly increased in the SAH group (P < 0.01).

Conclusions: The results of the present study suggest that SAH in the rabbits could induce NF-kappaB and proinflammatory cytokines activation in the intestine, which is associated with morphological changes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Appetite
  • Body Weight
  • Electrophoretic Mobility Shift Assay
  • Enteritis / etiology*
  • Enteritis / immunology*
  • Enteritis / pathology
  • Immunohistochemistry
  • Intercellular Adhesion Molecule-1 / metabolism
  • Intestinal Mucosa / immunology
  • Intestinal Mucosa / metabolism
  • Intestinal Mucosa / pathology
  • Leukocytes / pathology
  • Male
  • NF-kappa B / metabolism
  • Rabbits
  • Subarachnoid Hemorrhage / complications*
  • Subarachnoid Hemorrhage / immunology*
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • NF-kappa B
  • Tumor Necrosis Factor-alpha
  • Intercellular Adhesion Molecule-1