Related Experiment Video

Updated: Aug 7, 2026

Fixed Volume or Fixed Pressure: A Murine Model of Hemorrhagic Shock
16:31

Fixed Volume or Fixed Pressure: A Murine Model of Hemorrhagic Shock

Published on: June 6, 2011

Mesenteric lymph is responsible for post-hemorrhagic shock systemic neutrophil priming

R J Gonzalez1, E E Moore, D J Ciesla

  • 1Department of Surgery, Denver Health Medical Center, Colorado 80204, USA.

The Journal of Trauma
|December 12, 2001
PubMed
Abstract

Insights

Diversion of mesenteric lymph before hemorrhagic shock prevents neutrophil priming and lung injury. This finding highlights the role of lymph in shock-induced organ damage and suggests new therapeutic targets for multiple organ failure.

Area of Science:

  • Surgical Research
  • Trauma Pathophysiology
  • Immunology

Background:

  • Splanchnic hypoperfusion following hemorrhagic shock is a key factor in multiple organ failure (MOF).
  • Early neutrophil (PMN) priming post-injury indicates patients at risk for MOF.
  • Mesenteric lymph, collected after shock, has been shown to prime human neutrophils in vitro.

Purpose of the Study:

  • To investigate if diverting mesenteric lymph before hemorrhagic shock can prevent systemic PMN priming and subsequent lung injury.
  • To test the hypothesis that lymphatic diversion abrogates PMN priming and lung inflammation.

Main Methods:

  • Hemorrhagic shock (MAP 40 mm Hg x 30 min) and resuscitation were induced in rats with and without mesenteric lymphatic duct diversion.
  • Surface expression of CD11b on neutrophils was measured via flow cytometry to assess PMN priming.
  • Lung myeloperoxidase (MPO) levels and Evans blue lung leak were measured to evaluate PMN sequestration and lung injury.

Main Results:

  • Hemorrhagic shock significantly increased PMN CD11b expression, which was abrogated by lymphatic diversion.
  • Lung PMN accumulation (MPO levels) and lung leak (Evans blue) were significantly reduced in animals with lymphatic diversion compared to those without.
  • Lymphatic diversion returned lung injury markers to sham levels.

Conclusions:

  • Mesenteric lymph plays a crucial role in priming circulating neutrophils after hemorrhagic shock, leading to lung inflammation and injury.
  • Diversion of mesenteric lymph effectively prevents these pathological events.
  • Targeting PMN-priming agents in mesenteric lymph may offer novel therapeutic strategies for post-injury MOF.

More Related Videos

Visualization of Neutrophil Extracellular Traps in Mesenteric Venules After Mesenteric Ischemia-Reperfusion Injury via Intravital Microscopy07:05

Visualization of Neutrophil Extracellular Traps in Mesenteric Venules After Mesenteric Ischemia-Reperfusion Injury via Intravital Microscopy

Published on: September 27, 2024

Murine Mesenteric Lymphadenectomy for Selective Disruption of Lymphatic Communication with Region-Specific Gut07:27

Murine Mesenteric Lymphadenectomy for Selective Disruption of Lymphatic Communication with Region-Specific Gut

Published on: December 30, 2025

Related Concept Videos

Inflammation01:38

Inflammation

Overview
Secondary Lymphoid Organs01:15

Secondary Lymphoid Organs

Secondary organs, including lymph nodes, the spleen, and mucosa-associated lymphoid tissue (MALT), work harmoniously to protect us from disease and infection.
The spleen is a vital organ in the lymphatic system, nestled in the upper left side of the abdomen. It is composed of two primary regions: the red pulp and the white pulp, each having distinct functions. The red pulp performs a significant role in blood filtration. It efficiently purges the blood of old or damaged red blood cells and...
Acute Inflammation I: Inflammatory Response01:26

Acute Inflammation I: Inflammatory Response

Acute inflammation is a rapid, short-lived physiological response to tissue injury or infection, designed to eliminate harmful agents and initiate repair. This tightly regulated process typically lasts from minutes to several days and is triggered by factors such as microbial invasion, physical trauma, or chemical injury.Recognition and Mediator ReleaseThe inflammatory response begins when resident immune cells—such as mast cells, macrophages, and dendritic cells—detect damage-associated...
Acute Inflammation II: Cellular Phase01:26

Acute Inflammation II: Cellular Phase

The cellular phase of acute inflammation is a tightly orchestrated sequence of events that recruits leukocytes, primarily neutrophils, to sites of tissue injury or infection. Following the initial vascular changes, this phase ensures effective immune cell migration, activation, and function at the affected site to eliminate pathogens and initiate tissue repair.Leukocyte Recruitment CascadeLeukocyte recruitment happens in four steps: margination, adhesion, transmigration, and chemotaxis. Reduced...
Acute Inflammation III: Local and Systemic Effects01:25

Acute Inflammation III: Local and Systemic Effects

Acute inflammation produces a coordinated set of local and systemic changes that limit injury, eliminate pathogens, and initiate repair. These responses arise within minutes of infection, trauma, or chemical insult and are driven by vascular alterations and leukocyte-derived mediators. When the stimulus resolves, the reaction typically abates within days.Local EffectsAt the site of injury, arteriolar vasodilation increases blood flow, resulting in redness and warmth. Simultaneously, increased...
Secondary Spinal Cord Injury llI: Pathophysiology01:25

Secondary Spinal Cord Injury llI: Pathophysiology

Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...