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Updated: Aug 7, 2026
Rodent Model of Intestinal Ischemia-Reperfusion Injury via Occlusion of the Superior Mesenteric Artery
Published on: October 20, 2023
Shunting of the microcirculation after mesenteric ischemia and reperfusion is a function of ischemia time and
Michael Lauterbach1, Georg Horstick, Nicola Plum
1Institute for Neurosurgical Pathophysiology, Johannes Gutenberg-University Mainz, Mainz, Germany. mlauterbach@rics.bwh.harvard.edu
Objective:
Shunting of the microcirculation contributes to the pathology of sepsis and septic shock. The authors address the hypothesis that shunting of the microcirculation occurs after superior mesenteric artery occlusion (SMAO) and reperfusion, and explore functional consequences.
Methods:
Spontaneously breathing animals (rats) (n = 30) underwent SMAO for 0 (controls), 30 (SMAO_30) or 60 min (SMAO_60) followed by reperfusion (4 h) with normal saline. Leukocyte-endothelial interactions in mesenteric venules were quantified in an exteriorized ileal loop using intravital microscopy. Abdominal blood flow was recorded continuously, and arterial blood gases were analyzed at intervals. The above groups were matched by comparable groups with continuous superior mesenteric artery blood flow measurements and without exteriorizing an ileal loop (controls*, SMAO_30*, SMAO_60*).
Results:
Adherent leukocytes increased shortly after reperfusion in ischemia groups, and plateaued in these groups. Centerline velocity in the recorded venules was significantly reduced after reperfusion down to low-flow/no-flow in SMAO_60 as compared to SMAO_30 and controls, whereas perfusion of the SMA and ileal vessels persisted. The microcirculatory changes in SMAO_60 were accompanied by progressive metabolic acidosis, substantially larger volumes of intravenous fluids needed to support arterial blood pressure and significantly reduced survival (30%). SMA blood flow increased in relation to abdominal blood flow after reperfusion in SMAO_60*, and remained constant in SMAO_30* and controls*. Survival was 80% in SMAO_60*.
Conclusion:
Shunting of the microcirculation can be observed after SMAO for 60 min and reperfusion, and contributes significantly to the pathology of mesenteric ischemia and poor outcome.
Insights
Superior mesenteric artery occlusion (SMAO) for 60 minutes followed by reperfusion causes microcirculatory shunting, leading to mesenteric ischemia and reduced survival. This shunting impacts sepsis and septic shock pathology.
Area of Science:
- Physiology
- Surgical Pathology
- Vascular Biology
Background:
- Microcirculatory shunting is a key factor in sepsis and septic shock.
- Understanding shunting after mesenteric ischemia is crucial for improving patient outcomes.
Purpose of the Study:
- To investigate the occurrence of microcirculatory shunting following superior mesenteric artery occlusion (SMAO) and reperfusion.
- To explore the functional consequences of this shunting on mesenteric ischemia.
Main Methods:
- Rats underwent SMAO for 0, 30, or 60 minutes, followed by reperfusion.
- Intravital microscopy quantified leukocyte-endothelial interactions in mesenteric venules.
- Blood flow and arterial blood gases were monitored; some groups had continuous blood flow measurements without ileal loop exteriorization.
Main Results:
- Leukocyte adhesion increased post-reperfusion, particularly in the 60-minute occlusion group (SMAO_60).
- Centerline velocity decreased significantly in SMAO_60, leading to low-flow/no-flow states.
- SMAO_60 was associated with metabolic acidosis, increased fluid requirements, and reduced survival (30% vs. 80% in a separate SMAO_60* group).
Conclusions:
- Microcirculatory shunting occurs after 60 minutes of SMAO and reperfusion.
- This shunting significantly contributes to the pathology of mesenteric ischemia and poor outcomes.
- Findings highlight the role of shunting in the pathophysiology of conditions like sepsis.
