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- W1982188613 abstract "We tested the hypothesis that inducible isoform of nitric oxide synthase (iNOS)-derived nitric oxide (NO) inhibits oxygen consumption (Vo2) in human intestine resected for necrotizing enterocolitis (NEC). Each NEC resection specimen was divided into two sections based on histologic appearance: healthy or diseased. Intestine removed from infants for reasons other than NEC was used as control. The tissue injury score (0–6, with 6 indicating complete necrosis) was 0.4 ± 0.2 in control tissue, 1.2 ± 0.4 in NEC-healthy tissue, and 4.6 ± 0.5 in NEC-diseased tissue. Prominent iNOS staining was present in villus enterocytes in NEC-healthy tissue but not in the other tissue types. Intestinal Vo2 (per direct oximetry, in nM O2/min/g) was significantly greater in control tissue than in NEC-healthy or NEC-diseased tissues. Accumulation of NO into buffer bathing intestinal slices (in nM NO/μL/g) was greater in NEC-healthy tissue than control or NEC-diseased tissues. The specific iNOS antagonist l-Nω-(1-iminoethyl)-lysine (l-NIL) reduced buffer NO concentration 76% and increased Vo2 by 90% in NEC-healthy tissue; however, l-NIL had no effect on NO or Vo2 in control or NEC-diseased tissue. Addition of exogenous NO via S-nitroso-N-acetylpenicillamine depressed Vo2 in NEC-healthy and control tissues but not NEC-diseased tissue. A significant correlation was present between buffer NO concentration and Vo2 in NEC-healthy tissue. We conclude that iNOS-derived NO suppresses Vo2 in intestine resected for NEC that demonstrates a relatively normal histology on light microscopy." @default.
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- W1982188613 date "2006-04-01" @default.
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- W1982188613 title "Intestinal O2 Consumption in Necrotizing Enterocolitis: Role of Nitric Oxide" @default.
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- W1982188613 doi "https://doi.org/10.1203/01.pdr.0000203094.27615.5f" @default.
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