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Murine Mesenteric Lymphadenectomy for Selective Disruption of Lymphatic Communication with Region-Specific Gut
Published on: December 30, 2025
Mesenteric lymph duct ligation improves survival in a lethal shock model
Chirag D Badami1, Maheswari Senthil, Francis J Caputo
1Department of Surgery, New Jersey Medical School, University of Medicine and Dentistry of New Jersey, Newark, New Jersey 07103, USA.
Shock (Augusta, Ga.)
|May 23, 2008
Summary
Factors from the gut, transported via mesenteric lymph, significantly increase mortality in a lethal splanchnic artery occlusion (SAO) shock model. Blocking these gut factors improves survival and reduces shock severity.
Area of Science:
- Gastroenterology
- Surgical Shock Research
- Immunology
Background:
- Splanchnic artery occlusion (SAO) shock is a lethal condition.
- Factors released from the gut are suspected to contribute to SAO-induced mortality.
- The role of mesenteric lymph in transporting these factors is unclear.
Purpose of the Study:
- To test the hypothesis that gut-derived factors in mesenteric lymph contribute to mortality in a lethal SAO shock model.
- To investigate the impact of blocking these factors on survival and physiological responses.
Main Methods:
- A lethal SAO shock model was established in male Sprague-Dawley rats.
- Mesenteric lymph duct ligation (LDL) was performed to prevent lymph transport.
- Survival rates, blood pressure, plasma nitrite/nitrate levels, and hepatic inducible nitric oxide synthase (iNOS) protein levels were measured.
Main Results:
- LDL significantly improved 24-h and 7-day survival rates after SAO (0% vs. 60% at 24h; P < 0.05).
- LDL treatment blunted the hypotensive response to SAO.
- LDL abrogated the SAO-induced increase in plasma nitrite/nitrate and hepatic iNOS induction (P < 0.05).
- Unexpected variability in rat resistance and seasonal influences on results were noted.
Conclusions:
- Factors carried in the mesenteric lymph significantly contribute to mortality in lethal SAO shock.
- Blocking mesenteric lymph transport offers a protective effect against SAO-induced shock and mortality.
- The findings implicate gut-derived factors and iNOS in the pathophysiology of SAO shock.
