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Updated: Jun 16, 2026
A Swine Model of Neonatal Asphyxia
Published on: October 11, 2011
An animal model of necrotizing enterocolitis induced by infant formula and ischemia in developing piglets
K D Crissinger1, D L Burney, O R Velasquez
1Department of Pediatrics, Louisiana State University Medical Center, Shreveport.
Insights
Infant formula fat content is crucial for necrotizing enterocolitis development in piglets. High-fat preterm formula combined with ischemia/reperfusion creates a necrotizing enterocolitis model, highlighting the role of lipids in intestinal injury.
Area of Science:
- Gastroenterology
- Neonatal Research
- Animal Models
Background:
- The lipid component of piglet formula (0.5% fat) increases mucosal permeability in neonates after ischemia/reperfusion.
- Necrotizing enterocolitis (NEC) is a serious condition in premature infants, with formula composition potentially influencing its development.
Purpose of the Study:
- To investigate if infant formulas (3.5% fat) and ischemia/reperfusion induce an animal model of NEC in piglets.
- To determine if NEC injury is dependent on the fat composition of the infant formula.
Main Methods:
- Plasma-to-lumen clearance of 51Cr-EDTA and jejunoileal morphology were assessed in piglets.
- Luminal perfusion with preterm, term, and delipidated preterm formulas was performed before and after ischemia/reperfusion.
- Ileal segments were superfused with formulas without ischemia to evaluate direct effects.
Main Results:
- Preterm formula led to higher clearances and significant hemorrhagic/necrotic injury post-ischemia compared to delipidated formula.
- Delipidated formula resulted in minimal injury, indicating the protective role of lipid removal.
- Superfusion with preterm formula alone caused hyperemia and hemorrhage in villi.
Conclusions:
- Luminal perfusion with preterm infant formula and ischemia/reperfusion effectively models NEC in 1-day-old piglets.
- The lipid fraction of the infant formula is essential for inducing NEC in this animal model.
- Formula fat composition is a critical factor in the pathogenesis of ischemia/reperfusion-induced intestinal injury.
Background/Aims:
The lipid component of piglet formula (0.5% fat) causes increased mucosal permeability in 1-day-old piglets after ischemia/reperfusion. The present study examined if luminal exposure to infant formulas (3.5% fat) and ischemia/reperfusion result in an animal model of necrotizing enterocolitis and if injury is dependent on the formula fat composition.
Methods:
Plasma-to-lumen clearance of 51Cr-ethylenediamine-tetraacetic acid was measured, and morphology was evaluated during luminal perfusion with preterm, term, and delipidated preterm cow milk-based infant formulas before and after ischemia/reperfusion in 1-day-old and 1-month-old piglet jejunoileum. In a separate set of experiments, a 1-2-cm segment of ileum was exteriorized and opened to expose the mucosal surface, and the villi were superfused with the above formulas (no ischemia).
Results:
Before ischemia, clearances were markedly higher for intestinal loops perfused with preterm formula than for loops perfused with term and delipidated formulas in 1-day-old animals. After ischemia, clearances in loops perfused with preterm formula were significantly greater and grossly hemorrhagic and histologically necrotic compared with loops perfused with delipidated formula (minimal injury). Superfusion with preterm formula caused diffuse hyperemia and hemorrhage into intestinal villi.
Conclusions:
Luminal perfusion of 1-day-old piglet jejunoileum with predigested and bile acid-solubilized preterm infant formula, in combination with ischemia/reperfusion, produces an animal model of necrotizing enterocolitis, but only if the lipid fraction of the formula is present.
