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Enteral arginine does not increase superior mesenteric arterial blood flow but induces mucosal growth in neonatal pigs.

ABSTRACT: Arginine is an essential amino acid in neonates synthesized by gut epithelial cells and a precursor for NO that regulates vasodilatation and blood flow. Arginine supplementation has been shown to improve intestinal integrity in ischemia-reperfusion models and low plasma levels are associated with necrotizing enterocolitis. We hypothesized that enteral arginine is a specific stimulus for neonatal intestinal blood flow and mucosal growth under conditions of total parenteral nutrition (TPN) or partial enteral nutrition (PEN). We first tested the dose dependence and specificity of acute (3 h) enteral arginine infusion on superior mesenteric artery (SMA) blood flow in pigs fed TPN or PEN. We then determined whether chronic (4 d) arginine supplementation of PEN increases mucosal growth and if this was affected by treatment with the NO synthase inhibitor, N(G)-nitro-l-arginine methyl ester (L-NAME). Acute enteral arginine infusion increased plasma arginine dose dependently in both TPN and PEN groups, but the plasma response was markedly higher (100-250%) in the PEN group than in the TPN group at the 2 highest arginine doses. Baseline SMA blood flow was 90% higher in the PEN (2.37 ± 0.32 L?kg(-1)?h(-1)) pigs than in the TPN pigs (1.23 ± 0.17 L?kg(-1)?h(-1)), but was not affected by acute infusion individually of arginine, citrulline, or other major gut fuels. Chronic dietary arginine supplementation in PEN pigs induced mucosal growth in the intestine, but this effect was not prevented by treatment with L-NAME. Intestinal crypt cell proliferation, protein synthesis, and phosphorylation of mammalian target of rapamycin and p70S6 kinase were not affected by dietary arginine. We conclude that partial enteral feeding, but not acute enteral arginine, increases SMA blood flow in the neonatal pig. Furthermore, supplementing arginine in partial enteral feeding modestly increases intestinal mucosal growth and was NO independent.

SUBMITTER: Puiman PJ

PROVIDER: S-EPMC3001236 | biostudies-other | 2011 Jan

REPOSITORIES: biostudies-other

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Enteral arginine does not increase superior mesenteric arterial blood flow but induces mucosal growth in neonatal pigs.

Puiman Patrycja J PJ Stoll Barbara B van Goudoever Johannes B JB Burrin Douglas G DG

The Journal of nutrition 20101124 1

Arginine is an essential amino acid in neonates synthesized by gut epithelial cells and a precursor for NO that regulates vasodilatation and blood flow. Arginine supplementation has been shown to improve intestinal integrity in ischemia-reperfusion models and low plasma levels are associated with necrotizing enterocolitis. We hypothesized that enteral arginine is a specific stimulus for neonatal intestinal blood flow and mucosal growth under conditions of total parenteral nutrition (TPN) or part ...[more]

PMID: 21106927

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Project description:BackgroundIUGR infants are thought to have impaired gut function after birth, which may result in intestinal disturbances, ranging from temporary intolerance to the enteral feeding to full-blown NEC.In literature there is no consensus regarding the impact of enteral feeding on intestinal blood flow and hence regarding the best regimen and the best rate of delivering the enteral nutrition.Methods/designThis is a randomized, non-pharmacological, single-center, cross-over study including 20 VLBW infants. Inclusion criteria * Weight at birth ranging: 700-1501 grams * Gestational age up to 25 weeks and 6 days * Written informed consent from parents or guardians Exclusion criteria * Major congenital abnormality * Patients enrolled in other trials * Significant multi-organ failure prior to trial entry * Pre-existing cutaneous disease not allowing the placement of the NIRS' probe. In the first 24 hours of life, between the 48th and 72nd hours of life, and during Minimal Enteral Feeding, all infants' intestinal perfusion will be evaluated with NIRS and a Doppler of the superior mesenteric artery will be executed.At the achievement of an enteral intake of 100 mL/Kg/day the patients (IUGR and NON IUGR separately) will be randomized in 2 groups: Group A (n=10) will receive a feed by bolus (in 10 minutes); then, after at least 3 hours, they will receive the same amount of formula administered in 3 hours. Group B (n=10) will receive a feed administered in 3 hours followed by a bolus administration of the same amount of formula (in 10 minutes) after at least 3 hours. On the randomization day intestinal and cerebral regional oximetry will be measured via NIRS. Intestinal and celebral oximetry will be measured before the feed and 30 minutes after the feed by bolus during the 3 hours nutrition the measurements will be performed before the feed, 30 minutes from the start of the nutrition and 30 minutes after the end of the gavage. An evaluation of blood flow velocity of the superior mesenteric artery will be performed meanwhile. The infants of the Group A will be fed with continuous nutrition until the achievement of full enteral feeding. The infants of the Group B will be fed by bolus until the achievement of full enteral feeding.DiscussionEvaluations of intestinal oximetry and superior mesenteric artery blood flow after the feed may help in differentiating how the feeding regimen alters the splanchnic blood flow and oxygenation and if the changes induced by feeding are different in IUGR versus NON IUGR infants.Trial registration numberNCT01341236.

Project description:Inflammation in the premature intestine is a key factor that leads to the development of necrotizing enterocolitis (NEC). Activation of nuclear factor kappa B (NF-?B) and subsequent inflammation increases the severity of NEC. The aim of this study was to investigate the early temporal expression of inflammatory markers and activation of NF-?B in a neonatal rat model of NEC.Pre- and full-term newborn Sprague-Dawley rat pups were sacrificed at birth, 1.5, 4, 8, and 24 hours after receiving their first feed. Control pups were vaginally delivered and mother fed; NEC was induced by a combination of gavage feeding formula, hypoxia, and enteral lipopolysaccharide (LPS); and formula fed pups were fed every 4 hours with infant formula. Ileal tissue was collected for immunohistochemistry, real-time polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay. Serum was collected for cytokine content. Fold change of expression of inducible nitric oxide synthase (iNOS), interleukin (IL)-1?, IL-6, tumor necrosis factor-? (TNF-?), IL-10, NF-?B p65, and I?B? used RT-PCR. Data were analyzed by paired two-tailed t test, expressed as mean ± standard error of the mean, and p ? 0.05 considered significant.No histologic injury was evident in ileal sections. At 1.5 h, iNOS expression increased twofold over control in NEC pups (2.1 vs. 1.0, p ? 0.05) and remained elevated at 24 h (0.7 vs. 9.4, p ? 0.05). IL-1? and IL-6 reached a peak at 24 h in NEC tissue compared with control. IL-10 expression rose in NEC pups after 4 h of insult and remained elevated in formula and NEC stressed pups. Coincident with an increase in p65 translocation into the nucleus and a reduction of I?B? detected in the cytoplasm, increased transcription of I?B? occurs.These findings suggest that NF-?B activation initiates inflammation early in the course of NEC resulting in increased proinflammatory protein expression, underscoring the importance of the inflammatory response in this NEC model, which precedes evidence of histological injury.

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Enteral arginine does not increase superior mesenteric arterial blood flow but induces mucosal growth in neonatal pigs.

Publications

Enteral arginine does not increase superior mesenteric arterial blood flow but induces mucosal growth in neonatal pigs.

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