Necrotizing enterocolitis (NEC) is an acute inflammatory disease of the intestine which primarily affects preterm infants and is a leading cause of morbidity and mortality in the neonatal intensive care unit. From a clinical standpoint, and during the early course of the disease, NEC can be difficult to distinguish from other diseases and conditions common to the preterm infant, and this warrants the need for specific disease biomarkers. The pathogenesis of NEC is only partly understood but likely involves an altered intestinal barrier immune response to feeding and the developing microbiome. Recent evidence points toward a role of the enteric nervous system in NEC pathogenesis. In this issue, Meister and colleagues use a rodent model of NEC to demonstrate that NEC is associated with diminished vagal tone, as determined by decreased high‐frequency heart rate variability (HF‐HRV), and altered myenteric nitrergic inhibitory neurotransmission. These results augment their previous findings that describe decreased HF‐HRV in human preterm infants with NEC. This mini‐review provides a brief summary of clinical and pathophysiologic aspects of NEC with focus on certain aspects of neurogastroenterology.

Objective Eating difficulties coupled with cardiorespiratory spells delay acquisition of feeding milestones in convalescing neonates, and the mechanisms are unclear. Aims were to examine and compare the pharyngoesophageal–cardiorespiratory (PECR) response characteristics: (a) in control neonates and those with recurrent bradycardia spells; and (b) during pharyngeal stimulation when bradycardia occurs versus when no bradycardia occurs. Methods Preterm infants ( N = 40, 27 ± 3 weeks gestation), underwent concurrent pharyngoesophageal manometry, electrocardiography, respiratory inductance plethysmography, and nasal airflow thermistor to evaluate pharyngoesophageal motility, heart rate (HR), and respiration during graded abrupt pharyngeal sterile water stimuli. Infants with recurrent bradycardia ( N = 28) and controls ( N = 12) were evaluated at 38 (38–40) and 39 (38–40) weeks postmenstrual age, respectively. Comparisons were performed (a) between study and control groups; and (b) among HR responses of <80 BPM, 80–100 BPM, and >100 BPM. Results Overall, characteristics of PECR responses in infants with a history of recurrent bradycardia (vs. controls) did not differ ( p > .05). However, when pharyngeal stimulus induced severe bradycardia (<80 BPM): prolonged respiratory rhythm change, increased pharyngeal activity, increased esophageal dysmotility (as evidenced by prolonged esophageal inhibition and motor activity), and prolonged lower esophageal sphincter relaxation were noted (all p < .05). Conclusions In control infants and those with recurrent bradycardia, pharyngeal stimulation results in similar PECR response characteristics. However, when severe bradycardia occurs, PECR response characteristics are distinct. The mechanisms of severe bradycardia spells are related to abnormal prolongation of vagal inhibitory effects on cardiorespiratory rhythms in conjunction with prolonged esophageal inhibition and delays with terminal swallow.

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