Premium
A murine model for the study of edema induced intestinal contractile dysfunction
Author(s) -
Shah S. K.,
Mooreolufemi S. D.,
Uray K. S.,
Jimenez F.,
Walker P. A.,
Xue H.,
Stewart R. H.,
Laine G. A.,
Cox Jr C. S.
Publication year - 2010
Publication title -
neurogastroenterology and motility
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.489
H-Index - 105
eISSN - 1365-2982
pISSN - 1350-1925
DOI - 10.1111/j.1365-2982.2010.01546.x
Subject(s) - edema , medicine , phosphorylation , intestinal mucosa , myosin light chain kinase , myeloperoxidase , endocrinology , microbiology and biotechnology , biology , inflammation
Background We have published extensively regarding the effects of edema on intestinal contractile function. However, we have found the need to expand our model to mice to take advantage of the much larger arsenal of research support, especially in terms of transgenic mouse availability and development. To that end, we have developed and validated a hydrostatic intestinal edema model in mice. Methods Male C57 Black 6 mice were subjected to a combination of high volume crystalloid resuscitation and mesenteric venous hypertension in an effort to induce hydrostatic intestinal edema. Wet to dry ratios, myeloperoxidase activity, mucosal injury scoring, STAT‐3 nuclear activation, phosphorylated STAT‐3 levels, NF‐κB nuclear activation, myosin light chain phosphorylation, intestinal contractile activity, and intestinal transit were measured to evaluate the effects of the model. Key Results High volume crystalloid resuscitation and mesenteric venous hypertension resulted in the development of significant intestinal edema without an increase in myeloperoxidase activity or mucosal injury. Edema development was associated with increases in STAT‐3 and NF‐κB nuclear activation as well as phosphorylated STAT‐3. There was a decrease in myosin light chain phosphorylation, basal and maximally stimulated intestinal contractile activity, and intestinal transit. Conclusion & Inferences Hydrostatic edema in mice results in activation of a signal transduction profile that culminates in intestinal contractile dysfunction. This novel model allows for advanced studies into the pathogenesis of hydrostatic edema induced intestinal contractile dysfunction.