TY - JOUR
T1 - Intestinal O2 consumption in necrotizing enterocolitis
T2 - Role of nitric oxide
AU - Nowicki, Philip T.
AU - Reber, Kristina M.
AU - Giannone, Peter J.
AU - Nankervis, Craig A.
AU - Hammond, Sue
AU - Besner, Gail E.
AU - Caniano, Donna A.
PY - 2006/4
Y1 - 2006/4
N2 - 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 O 2/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-N ω-(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 Vo 2 in NEC-healthy and control tissues but not NEC-diseased tissue. A significant correlation was present between buffer NO concentration and Vo 2 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.
AB - 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 O 2/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-N ω-(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 Vo 2 in NEC-healthy and control tissues but not NEC-diseased tissue. A significant correlation was present between buffer NO concentration and Vo 2 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.
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U2 - 10.1203/01.pdr.0000203094.27615.5f
DO - 10.1203/01.pdr.0000203094.27615.5f
M3 - Article
C2 - 16549519
AN - SCOPUS:33646680768
SN - 0031-3998
VL - 59
SP - 500
EP - 505
JO - Pediatric Research
JF - Pediatric Research
IS - 4 PART 1
ER -