Tissue from patients with NEC can be informative

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Necrotizing entercolitis (NEC) remains an enigmatic disease associated primarily with prematurity. Hypotheses related to feeding, infection and vascular perfusion abnormalities have been proposed as contributing to the pathophysiology of NEC. Coagulation necrosis of the intestine at resection or autopsy is diagnostic of NEC but provides few clues to pathogenesis. While vasoactive and inflammatory mediators are increased in the circulation of infants with NEC, their importance to the tissue of interest – the gut – is never clear. Nowicki et al hypothesized that the potent vasoconstrictor endothelin-1 contributed to the gut injury. They assayed endothelin-1 concentrations in resected gut from NEC patients and compared levels in necrotic gut, gut adjacent to the necrosis and gut that appeared normal at the margin of resection. Endothelin-1 was increased in the gut tissue adjacent to the necrosis. They then made innovative measurements of arteriolar responses to endothelin 1 receptor antagonists using tissue recovered at surgery. Subserosal arterioles from gut adjacent to the necrosis vasodilated in response to a endothelin-1 receptor antagonist while arterioles from the more normal gut from NEC patients and gut from control patients did not. The use of resected gut from NEC patients to evaluate pathogenesis may be a very helpful experimental strategy.