Altered nitric oxide production in the premature gut may increase susceptibility to intestinal damage in necrotizing enterocolitis.

Background/purpose: Nitric oxide (NO) mediates enteric smooth muscle relaxation and mucosal protection. The authors have identified an ontogenically determined pattern of enteric NO neural maturation that may render the distal gut of premature piglets susceptible to injury.

Methods: NO synthase (cNOS and iNOS) activities were measured in the developing piglet gut wall and compared with gut from an intraluminal model of necrotizing enterocolitis (NEC) at different times.

Results: In premature animals, iNOS activity was significantly higher 3 hours after NEC induction compared with similarly treated 3-day-old piglets. INOS levels continued to rise 6 hours after NEC induction in prematures. Premature animals (labor induced by prostaglandins) failed to show such a rise in iNOS. In 3 day olds, iNOS levels increased significantly 16 hours after injury compared with the 3-hour group.

Conclusions: iNOS production increases in premature piglets with NEC compared with full-term NEC animals and continues to rise in the presence of intestinal damage regardless of developmental status. Maternal administration of prostaglandins attenuates this rise in iNOS activity. Elevated NO production in premature gut may contribute to increased susceptibility to damage in NEC.