A comprehensive review of necrotizing enterocolitis (NEC) is provided; including history, biological basis and frequently asked questions. In addition, a system of improved NEC classification is explained in detail (consisting of five NEC subsets and four NEC-like diseases), to aid the bedside clinician in therapy and prevention. The authors offer opinion for therapeutics in italics at the end of each definition.
The mechanisms that regulate relaxation of the fetal ductus arteriosus (DA) and its postnatal constriction are the subject of ongoing studies. Using pressure myography, a pattern of rhythmic oscillatory contractions termed vasomotion was observed in the isolated DA of preterm (day 15) fetal mice. Vasomotion was enhanced by oxygen-induced DA constriction and other contractile agents, and diminished by vasodilatory stimuli or inhibition of chloride channels. The DA of late preterm (day 17) or term (day 19) gestation fetal mice did not exhibit vasomotion. These studies establish the stage-specific presence of vasomotion in the DA of fetal mice and suggest that complex events contribute to intrinsic mechanisms for control of fetal DA tone.
BACKGROUND Mucosal apoptosis is the initiating event in models of necrotizing enterocolitis (NEC) within rodents. It is possible there are species-specific differences that make apoptosis a more prominent feature of NEC in rodents than in humans. HYPOTHESIS A lower threshold for mucosal apoptosis in the rodent distal intestine might have evolutionary advantages (via enhanced opsonization with the neonatal Fc receptor [FcRn]), since many short-gestation mammals are comparatively premature (histomorphologically) but are protected from NEC by breast milk. METHODS We utilized a rat intestinal epithelial cell (IEC-18) model to determine if cell death alters FcRn - IgG binding, and rodent models of NEC to determine if cell death results in increased opsonization of IgG. Cultured IEC-18 cells were treated with H2O2 and analyzed. Neonatal Sprague-Dawley rats were cold and hypoxia stressed and intestinal sections were frozen for analysis. RESULTS IgG binding was increased in H2O2-treated cells. Co-incubation of treated cells with either insulin-like growth factor or tunicamycin decreased IgG binding. Sprague-Dawley rats formula fed with exogenous bacteria showed a significant decrease in intestinal FcRn mRNA but increased ileal IgG binding. CONCLUSIONS We speculate that FcRn plays a role in passive opsonization and subsequent bacterial pathogen clearance, making rodents resistant to NEC.
