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A murine model for the study of edema induced intestinal contractile dysfunction
S K Shah1, S D Moore-Olufemi, K S Uray
1Department of Pediatric Surgery, University of Texas Medical School at Houston, Houston, TX 77030, USA.
Neurogastroenterology and Motility
|July 2, 2010
Summary
A new mouse model of hydrostatic intestinal edema was developed. This model shows edema causes intestinal dysfunction by activating specific signaling pathways, impacting contractile activity and transit.
Area of Science:
- Physiology
- Gastroenterology
- Edema Pathogenesis
Background:
- Extensive research exists on edema's effects on intestinal function.
- A need was identified to develop a mouse model for enhanced research capabilities, including transgenic models.
- A novel hydrostatic intestinal edema model in mice has been successfully developed and validated.
Purpose of the Study:
- To develop and validate a hydrostatic intestinal edema model in mice.
- To investigate the molecular and functional consequences of hydrostatic edema in the intestine.
- To establish a platform for studying edema-induced intestinal dysfunction.
Main Methods:
- Male C57 Black 6 mice were used.
- Hydrostatic intestinal edema was induced via high-volume crystalloid resuscitation and mesenteric venous hypertension.
- Measurements included wet/dry ratios, myeloperoxidase activity, mucosal injury, STAT-3 and NF-κB activation, myosin light chain phosphorylation, contractile activity, and intestinal transit.
Main Results:
- The model successfully induced significant intestinal edema without increasing myeloperoxidase activity or mucosal injury.
- Edema correlated with increased STAT-3 and NF-κB nuclear activation and STAT-3 phosphorylation.
- A decrease in myosin light chain phosphorylation, intestinal contractility, and transit was observed.
Conclusions:
- Hydrostatic edema in mice activates signal transduction pathways leading to intestinal contractile dysfunction.
- This validated mouse model provides a foundation for further research into the pathogenesis of hydrostatic edema-induced intestinal dysfunction.
