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Updated: Aug 23, 2026
Murine Mesenteric Lymphadenectomy for Selective Disruption of Lymphatic Communication with Region-Specific Gut
Published on: December 30, 2025
Lymphatic diversion prevents myocardial edema following mesenteric ischemia/reperfusion
Charles S Cox1, Uwe M Fischer, Steven J Allen
1Center for Microvascular and Lymphatic Studies, Department of Surgery, University of Texas--Houston Medical School, Houston, Texas, USA.
Objective:
Mesenteric ischemia/reperfusion (I/R) is associated with cardiac dysfunction. Mesenteric lymph primes polymorphonuclear leukocytes (PMNs) for increased superoxide release following I/R. We hypothesized that mesenteric I/R causes myocardial edema resulting in myocardial dysfunction, and that diverting mesenteric lymph would preserve myocardial function.
Methods:
Two canine groups were studied: lymphatic diversion (LD) and no lymphatic diversion (No LD). Preload recruitable stroke work, +/-dp/dt(max), isovolumic relaxation (tau), cardiac output, and myocardial water content (MWC) were determined. I/R consisted of 60 min of ischemia followed by 180 min of reperfusion. Myocardial myeloperoxidase (MPO) was measured as an index of PMN leukosequestration. In addition, mesenteric lymph harvested after I/R was infused into normal canines and all variables measured.
Results:
MWC increased from baseline in No LD. Tau and -dp/dt(max) were significantly affected in No LD, but not in LD. After mesenteric I/R, mesenteric lymph primed PMNs for increased superoxide production. Lymph diversion resulted in significantly lower myocardial MPO. With reinfusion of I/R lymph, MWC and tau increased. MPO was also increased post I/R mesenteric lymph reinfusion.
Conclusions:
Our data indicate that myocardial dysfunction after mesenteric I/R is due to lymph-induced, PMN-mediated microvascular alterations and myocardial edema.
Insights
Diverting mesenteric lymph prevents cardiac dysfunction after ischemia/reperfusion (I/R) injury. Mesenteric lymph, activated by I/R, causes myocardial edema and polymorphonuclear leukocyte (PMN) activation, leading to heart dysfunction.
Area of Science:
- Cardiovascular Physiology
- Gastrointestinal Surgery
- Immunology
Background:
- Mesenteric ischemia/reperfusion (I/R) injury is linked to cardiac dysfunction.
- Mesenteric lymph, activated by I/R, primes polymorphonuclear leukocytes (PMNs) for enhanced superoxide release.
- This priming contributes to systemic inflammatory responses and organ damage.
Purpose of the Study:
- To investigate if mesenteric I/R induces myocardial edema and subsequent cardiac dysfunction.
- To determine if diverting mesenteric lymph can preserve myocardial function following I/R.
- To elucidate the role of lymph-primed PMNs in I/R-induced myocardial injury.
Main Methods:
- Canine models with and without lymphatic diversion (LD) were used.
- Hemodynamic parameters (preload recruitable stroke work, +/-dp/dt(max), cardiac output) and myocardial water content (MWC) were measured.
- Myeloperoxidase (MPO) assessed PMN infiltration; I/R lymph reinfusion studies were conducted.
Main Results:
- No LD group showed increased MWC and impaired relaxation (tau), unlike the LD group.
- Mesenteric I/R lymph primed PMNs for increased superoxide production and elevated myocardial MPO.
- Reinfusion of I/R lymph increased MWC, impaired tau, and elevated MPO in normal canines.
Conclusions:
- Mesenteric I/R triggers lymph-mediated PMN activation.
- This activation leads to microvascular changes and myocardial edema, causing cardiac dysfunction.
- Lymphatic diversion is a potential therapeutic strategy to mitigate I/R-induced cardiac injury.
