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Endothelin-1 in human intestine resected for necrotizing enterocolitis
Philip T Nowicki1, David J Dunaway, Craig A Nankervis
1Center for Cell and Vascular Biology, Columbus Children's Research Institute, Department of Pediatrics, Division of Neonatology, Ohio State University, USA. nowickip@pediatrics.ohio-state.edu
The Journal of Pediatrics
|June 24, 2005
Summary
Necrotizing enterocolitis (NEC) in preterm infants is linked to higher endothelin-1 (ET-1) levels in the gut. Blocking ET-1 receptors reversed vasoconstriction in affected intestinal arterioles, suggesting a therapeutic target for NEC.
Area of Science:
- Neonatal research
- Gastroenterology
- Vascular biology
Background:
- Necrotizing enterocolitis (NEC) is a severe gastrointestinal emergency in preterm infants.
- Endothelin-1 (ET-1) is a potent vasoconstrictor implicated in various vascular pathologies.
Purpose of the Study:
- To investigate elevated ET-1 concentrations in NEC-affected human preterm intestine.
- To determine ET-1's role in regulating blood flow within intestinal arterioles in NEC.
Main Methods:
- Human preterm intestinal tissue resected for NEC was analyzed for ET-1 concentration using ELISA.
- Histologic NEC scoring was performed on different intestinal zones.
- In vitro studies on subserosal arterioles assessed hemodynamic responses to ET-1 receptor blockade (BQ610).
Main Results:
- Significantly higher ET-1 tissue concentrations were found in NEC-affected intestinal zones compared to healthier regions.
- Arterioles from NEC-affected areas exhibited reduced flow and diameter, indicating vasoconstriction.
- Blockade of ET-1 A receptors successfully vasodilated arterioles from NEC-affected intestine, restoring normal blood flow parameters.
Conclusions:
- Elevated ET-1 levels are present in human preterm intestine with histologic evidence of NEC.
- ET-1 mediates vasoconstriction in intestinal arterioles affected by NEC.
- Targeting ET-1 receptors offers a potential therapeutic strategy for managing NEC-related vascular dysfunction.