Vascular disease in necrotizing enterocolitis

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Despite many years of clinical research and multiple animal models, the initiating factors and pathways for progression to necrotizing enterocolitis (NEC) remain essentially unknown. Decreased perfusion of the gut is thought to be central to the pathophysiological sequences that are suspected to occur in NEC. Nowicki et al previously published in this journal that microvessels adjacent to the region of acute NEC contained increased endothelin-1, a potent vasoconstrictor. Again using resected tissue from cases of NEC, this group reports that endothelial nitric oxide synthase was present in the vessels from patients with NEC but it did not generate NO to vasodilate the constricted arterioles. These studies using tissue from patients wtih NEC do not identify what initially causes NEC, but they do demonstrate clear abnormalities in vasoregulation once NEC is present. In an accompanying editorial, Rosemary Higgins reviews the many unresolved issues about this perplexing gut disease.

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