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Excess nitric oxide does not cause cellular, vascular, or mucosal dysfunction in the cat small intestine
P Kubes1, P H Reinhardt, D Payne
1Department of Medical Physiology, University of Calgary Medical Center, Alberta, Canada.
The American Journal of Physiology
|July 1, 1995
Summary
High concentrations of nitric oxide donors did not impair small bowel barrier function in vivo or in vitro. Exogenous nitric oxide even reduced inflammation-induced permeability, suggesting it is not cytotoxic to the gut barrier.
Area of Science:
- Gastroenterology
- Physiology
- Biomedical Science
Background:
- Overproduction of nitric oxide (NO) in the small bowel is implicated in inflammatory dysfunction.
- The cytotoxic effects of NO on vascular and mucosal barriers require further investigation.
Purpose of the Study:
- To determine if exogenous nitric oxide (NO) administration causes microvascular and mucosal barrier dysfunction.
- To assess the impact of NO donors on epithelial and endothelial cell permeability and injury.
Main Methods:
- Nitric oxide donors (CAS 754, SIN-1) were infused into feline ileum segments.
- Epithelial and vascular permeability were measured using 51Cr-EDTA clearance and protein clearance.
- In vitro studies assessed cell permeability and injury in endothelial and epithelial cell monolayers.
Main Results:
- Exogenous NO did not affect baseline epithelial permeability but reduced vascular protein clearance.
- Direct microvascular permeability measurements were unaffected by NO.
- NO did not increase cell permeability or cause injury in vitro.
- NO reduced, rather than exacerbated, platelet-activating factor-induced permeability.
Conclusions:
- High concentrations of exogenous nitric oxide do not compromise small bowel mucosal or microvascular barrier integrity.
- NO may have protective effects against inflammation-induced barrier dysfunction.